Obstetrics and Gynaecology Flashcards
Define stress incontinence
Involuntary leakage of urine on effort or exertion, or on sneezing/coughing
Risk factors for stress incontinence?
Increasing age, pregnancy and vaginal delivery, obesity, constipation, prolapse, hysterectomy, menopause and decreased oestrogen, family history, smoking, drugs eg ACEi
How to assess pelvic muscle tone?
Digitally
Use modified oxford grading system (0-5, rates strength of contraction)
What can you do initially to manage stress incontinence?
Lifestyle advice: decrease caffeine, weight loss if bmi ove 30, advice on fluid intake, smoking cessation, pelvic floor muscle training
3 months pelvic floor training then duloxetine/surgery consideration
What can be done in secondary care for stress incontinence?
Colposuspension, autologous rectus fascial sling, retro pubic mid-urethral mesh sling, intramural urethral bulking agents
Surgery is first line in secondary care. Can offer duloxetine as 2nd line
Describe an overactive bladder presentation
Urinary urgency associated with increased frequency and nocturia
Can be wet (incontinent) or dry (no incontinence)
Pathophysiology of overactive bladder?
Involuntary contractions of detrusor muscle during filling phase of micturition
Aetiology of overactive bladder?
Most=idiopathic
Can be a/w PD, MS, injury to pelvic/spinal nerves, drugs eg diuretics/antidepressants/hrt
How to manage overactive bladder initially?
Exclude/manage treatable causes
Lifestyle advice
Bladder training for at least 6 weeks
Then add in antimuscarinic eg oxybutynin/tolterodine/darifenacin
Mirabegron is another option (beta 3 adrenergic receptor agonist- relaxes sm and increases bladder capacity)
Secondary care options for overactive bladder?
Botulinum toxin type a injection into bladder wall
Percutaneous sacral nerve stimulation
Augmentation cystoplasty
Urinary diversion
Pathophysiology of uterovaginal prolapse
Pelvic floor muscles and ligaments stretch and weaken over time and can no longer support the uterus. The uterus slips down into or protrudes out of the vagina
Presentation of uterovaginal prolapse?
Tends to affect postmenopausal women who have had at least one vaginal delivery
Mild=normally asx
Mod-severe= heaviness/pulling in pelvis, tissue protruding from vagina, urinary sxs, trouble with bowel movements, feeling like they’re sitting on a small ball, sexual concerns
Symptoms tend to be worse later on in the day
Causes of weakened pelvic floor muscles?
Pregnancy, difficult labour, large baby, overweight, lower oestrogen after menopause, chronic constipation, chronic cough, repeated heavy lifting
Management of uterovaginal prolapse?
Self care measures, pessary, surgery (repair of tissues or hysterectomy). Kegel exercises very important
Difference between rectocele and cystocele?
Rectocele=posterior vaginal prolapse
Cystocele=anterior vaginal prolapse
Potential presentations of rectocele?
Small ones may be asx
Bulge of tissue, difficulty having bowel movement, sensation of rectal pressure or fullness, feeling of incomplete emptying, sexual concerns
Causes of rectocele?
Chronic constipation, chronic cough, repeated heavy lifting, overweight, more vaginal deliveries
management of rectocele?
Self care measures eg Kegel exercises
Pessary
Surgical repair may be considered (mesh patch inserted)
Pathophysiology of cystocele?
Bladder drops from normal position and pushes on wall in vagina- pelvic floor weakened or too much pressure on pelvic floor
Management of cystocele?
Mild cases typically are watch and wait
Pelvic floor muscle exercises
Pessary
May consider surgery
Types of female genital tract fistulae?
Vesicovaginal (bladder fistula, most common)
Uterovaginal
Urethrovaginal
Rectovaginal
Colovaginal
Enterovaginal (small intestine and vagina)
Why do fistulae develop?
Due to injury, surgery, infectoin or radiation treatment
Can occur as a result of prolonged childbirth
What are potential problems with vesicovaginal or rectovaginal fistulae?
Uncontrolled urinary or faecal incontinence or leakage out of the vagina
Treatment of genital tract fistulae?
surgery
Describe a fibroid
Most common benign tumour in women
Smooth muscle cells and fibroblasts accumulate to form a hard, round, whorled tumour in the myometrium
When do you get fibroids and why?
Develop during reproductive age as maintained by oestrogen and progestogen
Types of fibroid?
Subserosal (outer serosal surface of uterus and extend into peritoneal cavity, commonly asx)
Intramural (don’t extend into uterine/peritoneal cavities, may cause menorrhagia and dysmenorrhoea)
Submucosal (inner mucosal surface, extend into uterine cavity, cause significant menorrhagia, dysmenorrhoea and reduced fertility)
NB/ subserosal and submucosal may become pedunculated
Risk factors for fibroids?
What reduces risk?
RF: increasing age, early puberty, obesity, family history, black
Reduced risk: pregnancy and number of pregnancies
Complications of fibroids?
Abnormal uterine bleeding, compression or adjacent organs, infertility, pregnancy problems, torsion of pedunculated fibroid, red degeneration of fibroid (during 1st and 2nd trimester, fever, pain and vomiting)
Presentation of fibroids?
Menorrhagia, pelvic pain, abdo distension, pelvic pressure/discomfort, urinary symptoms, subfertility, non-specific bowel problems
Management of fibroids?
Doesn’t require management in most cases
If fibroid under 3cm: mirena coil is first line, if unsuitable can use tranexamic acid. NB/ can also use COCP but contraindicated when surgery might be involved.
Endometrial ablation can he used. As can uterine artery embolisation
Myomectomy or hysterectomy
If surgery: GnRH agonists (eg goserelin acetate) used before surgery to reduce size of fibroid and make them less likely to bleed.
Types of ovarian cysts?
Functional cysts (most common) Dermoid (teratomas- form from embryonic cells and can contain tissue eg hair/skin/teeth) Cystadenomas (on surface of ovary) Endometriomas
Complications of ovarian cysts?
Dermoid cysts and cystadenomas can grow large and move ovary therefore increasing chance of ovarian torsion Also rupture (severe pain and bleeding)
What investigations for ovarian cysts?
Pelvic exam Pregnancy test (+=?corpus luteum cyst) Pelvic USS Laparoscopy CA125 blood test (?malignancy)
Management of ovarian cysts?
Watchful waiting, oral contraceptives, surgery
What are functional cysts? What are the two types?
Cysts as a result of the menstrual cycle, when normal follicle continues to grow. Rarely painful, usually harmless and self limiting for 2-3 cycles
Follicular cyst and corpus luteum cyst (when follicle doesn’t rupture/release its egg or fluid accumulates inside follicle= corpus luteum grows into cyst)
Age distribution of ovarian torsion?
Bimodal :
15-30 and postmenopausal
Causes of ovarian torsion?
Hypermobility of ovary Adnexal mass (most lesions=dermoid cysts or paraovarian cysts)
Younger= developmental abnormalities
Adults=ovarian tumours, polycystic ovaries, adhesions
Presentation of ovarian torsion?
severe non specific lower abdo/pelvic pain (intermittent or sustained)
Nausea and vomiting
Adnexal tenderness
Commonly have increased WCC
Management of ?ovarian torsion?
Urgent USS
Urgent surgery to prevent ovarian necrosis
Most ovaries non-salvageable: salpingo-oophorectomy
If non-infarcted= surgical untwisting
What is lichen sclerosus?
Common chronic skin disorder- most often affects genital and perianal areas
Most common in women over 50
Thought to be autoimmune
Presentation of lichen sclerosus?
Crinkled/thickened white patches of skin that tend to scar
Vulval lichen sclerosus= primarily non hair bearing inner areas, localised or diffuse, never involves vaginal mucosa, can be v itchy and sore
Complications of lichen sclerosus?
Infections (thrush, herpes, S. aureus)
Increased risk of SCC
Management of lichen sclerosus?
Lifestyle measures eg wash gently, non soap cleanser, loose clothing
Topical steroid ointment eg clobetasol propionate 0.05%
Other topical tx= oestrogen cream, calcineurin inhibitor eg tacrolimus ointment
What are the types of cervical cancer?
SCC (70-80%) Cervical adenocarcinoma (up to 10%)
What virus is associated with cervical cancer? Which subtypes specifically?
Human papillomavirus (HPV) esp HPV16 and HPV18
What increases risk of HPV causing cervical cancer?
Co-infection with other STIs, smoking, high parity, young age at first pregnancy, FH, oral contraceptive pill for over 5 years, immunocompromised
What increases risk of contracting HPV?
Increased number of sexual partners, no condom use, age at first sexual intercourse
Presentation of cervical cancer?
Asx, non specific sxs;
Intermenstrual/postcoital/postmenopausal bleeding, blood-stained vaginal discharge, mucoid/purulent discharge, pelvic pain/dyspareunia
What things are in place to help prevent cervical cancer?
HPV vaccination at age 12-13 for girls
Cervical cancer screening: every 3 years after 24/25
Describe the stages of cervical cancer?
I (carcinoma restricted to cervix- either microscopic (1A1 and 1A2) or clinically visible (1B1 and 1B2))
II (beyond uterus but not into pelvic wall or into lower third of vagina)
III (onto pelvic sidewall, lower third of vagina)
IV (beyond true pelvis either adjacent organs or distant organs)
What is cervical intraepithelial neoplasia/CIN?
Pre-invasive cancer
Management of cervical cancer?
Conservative
Hysterectomy, lymphadenectomy
Chemoradiation (over 4cm)
Manage complications
How does endometrial cancer present?
Postmenopausal= vaginal bleeding and visible haematuria Pre-menopausal= abnormal bleeding
RFs for endometrial cancer?
Increasing age, unopposed oestrogne after menopause (not kept in balance by progestogen), overweight/obese (oestrogen produced in fatty tissue), nulliparous, on tamoxifen, high levels of insulin, PCOS, endometrial hyperplasia
What type are most endometrial cancers?
Adenocarcinoma
How to investigate ?endometrial cancer? What would treatment consist of?
Transvaginal USS then hysteroscopy and biopsy then staging with CXR/MRI/CT/bloods etc
Mx=hysterectomy, remove ovaries and fallopian tubes, may need radio/chemotherapy
Presentation of ovarian cancer?
IBS like symptoms- constantly bloated, abdominal distension, pelvic/abdo discomfort, early satiety/loss of appetite, urinary frequency/urgency
Also: indigestion, nausea, dyspareunia, bowel habit change, back pain, tiredness, unintentional weight loss
RFs for ovarian cancer?
Increasing age, FH, BRCA1/2, HRT, endometriosis, obesity, smoking, asbestos exposure
Investigations for ?ovarian cancer?
Management?
CA125 (blood test)
USS
CT/Xray/needle biopsy/laparoscopy
Mx= surgery and chemo
Describe staging of ovarian cancer?
i= ovary(ies) ii= into pelvis/womb iii= into peritoneum, bowel surface or lymph glands iv= distant organs
Presentation of vulval cancer?
Mostly in over 65s, rare
Persistent itch, pain/soreness/tenderness, bleeding, open sore, dysuria, mole on vulva
Most often affects inner edge of labia majora or labia minora
RFs for vulval cancer?
Increasing age, vulval intraepithelial neoplasia, HPV infection, lichen sclerosus, smoking, previous radiotherapy
What type of cancer is vaginal cancer?
SCC mostly (90%) 10% are adenocarcinomas
Presentation of vaginal cancer?
Very rare!
Asx, abnormal bleeding, abnormal discharge, dyspareunia, lump/growth, persistent vaginal itch
What is a hydatidiform mole? Two types-describe
Molar pregnancy- abnormal growth of trophoblasts
Complete= no formation of foetal tissue, placenta is abnormal and swollen Partial= maybe normal placental tissue, maybe formation of foetus (miscarried)
Presentation of hydatidiform mole?
Dark brown-bright red vaginal bleeding during 1st trimester, severe N/V, sometimes passage of grape-like cysts, pelvic pressure or pain
Pathophysiology of hydatidiform mole?
Egg fertilised by 1 or 2 sperm
Maternal chromosomes lost/inactivated (complete) or father provides 2 sets with mum’s 1 (partial)
Complications of hydatidiform mole?
Molar tissue may remain and continue to grow= gestational trophoblastic neoplasia (GTN)
High level of HCG
May develop cancerous form= choriocarcinoma
Investigating hydatidiform mole?
Management?
Ix= HCG, USS, other bloods Mx= non viable pregnancy will either miscarry of need surgery
Different management options for prolapse?
Pelvic floor muscle training, vaginal oestrogen, vaginal pessaries, pelvic floor repair, hysterectomy, sacroplexy or sacrospinous fixation (mesh and tape)
What is endometriosis?
Endometrial tissue grows outside of the uterus- commonly involves ovaries, fallopian tube and tissue lining pelvis
This tissue thickens, breaks down and bleeds but there is no way for the tissue to exit the body and so is trapped
Tissue becomes irritated and can form scar tissue and adhesions
If ovaries involved, cysts/endometriomas may form
Presentation of endometriosis?
Chronic pelvic pain often a/w periods Dysmenorrhoea Dyspareunia Pain on bowel movements or urination Excessive bleeding Infertility
How to diagnose endometriosis?
Pelvic exam, USS, MRI can point towards diagnose
Only way to formally diagnose= laparoscopy
How to manage endometriosis?
Simple analgesia= NSAIDs and tranexamic acid
Ovulation suppression (tricyclic COCP, Mirena coil, GnRH analogues)
Laser/diathermy ablation
Radical hysterectomy and oophorectomy
What increases marker CA125?
NOT vulval
Only one used in ovarian cancer
Also: adenomyosis, ascites, endometriosis, menstruation, breast cancer, ovarian cancer, ovarian torsion, endometrial cancer, liver disease, metastatic lung cancer
What is adenomyosis?
Uterine condition of ectopic endometrial tissue in the myometrium
RFs for adenomyosis?
High oestrogen exposure eg short menstrual cycles and early menarche, or treated with tamoxifen
Presentation of adenomyosis?
Most commonly asx and multiparous women of reproductive age
Potential sxs= dysmenorrhoea, menorrhagia, dyspareunia, chronic pelvic pain, menometrorrhagia
What are the 3 types of adenomyosis?
Diffuse, focal, cystic
What investigations for adenomyosis?
Management?
1st line=Uss, gold= pelvic MRI
Mx: similar to endometriois- GnRH agonist, hysterectomy
Define dysfunctional endometrial bleeding?
Abnormal uterine bleeding in absence of recognisable pelvic pathology, general medical disease or pregnancy
Mainly caused by imbalance in sex hormones
Abnormal may= intermenstrual, heavy, clots, bleeding>7 days, short or long cycles, spotting
When do you see lots of dysfunctional endometrial bleeding?
Early on in puberty
how to manage dysfunctional endometrial bleeding?
Oral contraceptives, or other hormonal contraceptives. Mostly a temporary condition- manage any anaemia
How is androgen insensitivity syndrome inherited?
X linked recessive
How does androgen insensitivity syndrome present?
Complete or partial where partial has more ambiguous px eg micropenis or clitoromegaly/hypospadias etc
External female phenotype, genotype is male
Undescended testes, female external genitalia, breast tissue, absence of internal female genitalia, lack of pubic hair/facial hair, taller than female average
Infertile and increased risk of testicular cancer
Primary amenorrhoea
What can be seen in the bloods of someone with androgen insensitivity syndrome?
Increased LH
Normal/raised FSH
Increased oestrogen
Normal/raised testosterone
How to manage androgen insensitivity syndrome?
Bilateral orchidectomy, oestrogen therapy, vaginal dilators/surgery to create adequate vaginal length
Raised as girls/women generally
Incidence of premature menopause
1 in 100 (occurring in under 40s)
Common menopause symptoms?
Hot flushes, night sweats, vaginal dryness, difficulty sleeping, low mood or anxiety, reduced libido, memory and concentration problems
What gonadotrophin is higher in menopause?
FSH
how to manage menopause?
HRT, simple measures for sweats/flushes, CBT, antidepressants, testosterone gel (libido), vaginal oestrogen, calcium/vit d/bisphosphonates (osteoporosis risk)
What is atrophic vaginitis?
When does it occur?
Thinning, drying and inflammation of vaginal walls due to decreased oestrogen
Occurs: perimenopause, menopause, surgical menopause, during breast feeding, contraceptive pills, pelvic radiation, chemo, breast cancer hormonal treatment
Describe GSM (genitourinary syndrome of menopause)
Dryness, burning, discharge, itching, burning/urinary/frequency, recurrent UTIs, incontinence, postcoital bleeding, dyspareunia, decreased vaginal lubrication during intercourse, shortening and tightening of vagina
Management of atrophic vaginitis?
Vaginal moisturisers, water-based lubricant, topical oestrogen, vaginal dilators, topical lidocaine, regular intercourse
Precocious and late menarche?
Precocious=under 9
Late= over 15 years
Describe physiology of menarche
Pulsatile GnRH from hypothalamus stimulates pituitary production of FSH and LH. This increases ovarian production of oestrogens (oestradiol and androgens).
Oestradiol causes maturation of ovarian follicles
Increased oestrogen causes uterine endometrial proliferation and eventually an LH surge, causing ovulation or rupture of dominant ovarian follicle
Progesterone (adrenal cortex and ovaries) causes thickening of endometrium
Presentation of endometrial polyps?
Irregular menstrual bleeding, intermenstrual bleeding, menorrhagia, bleeding after menopause, infertility
RFs for endometrial polyps?
Oestrogen dependent: peri/postmenopausal, hypertension, obesity, tamoxifen
How to investigate and manage endometrial polyps?
Ix: transvaginal USS, hysteroscopy, endometrial biopsy
Mx: watchful waiting, short term meds (progestins and GnRH agonists), surgical removal
Most common location for ectopic pregnancy?
Fallopian tube (tubal pregnancy)
RFs for ectopic pregnancy?
Previous ectopic pregnancy, inflammation or infection (STIs), fertility treatments, tubal surgery, birth control (IUD and tubal ligation/tubes tied), smoking
Presentation of ectopic pregnancy?
Positive pregnancy test, early presentation pregnancy (missed period, breast tenderness, nausea), light vaginal bleeding and pelvic pain
NB/ if blood leaks from fallopian tube may feel shoulder pain or urge to have bowel movement
Rupture if continued growth- shock and life threatening
How to manage an ectopic pregnancy?
Methotrexate injection for early ectopic without unstabke bleeding
Laparoscopy- salpingostomy/salpingectomy (ectopic/ectopic and tube removed)
Emergency surgery
Incidence of polycystic ovaries and polycystic ovary syndrom?
Polycystic ovaries= up to 33% of women of reproductive age
PCOS= 5-15% of women of reproductive age
Pathophysiology of PCOS?
Excess androgens (ovary theca cells- due to hyperinsulinaemia or increased LH) and insulin resistance > hyperinsulinaemia > increased androgens and decreased SHBG (sex hormone binding globulin) in liver, increased LH due to increased production (anterior pituitary) and increased oestrogen in some women (causing hyperplastic endometrium)
Presentation of PCOS?
Peripubertal -mid 20s
Oligomenorrhoea (under 9 periods/year), infertility/subfertility, acne and hirsutism, alopecia, obesity/difficulty losing weight, psych symptoms, sleep apnoea, may have acanthosis nigricans
Criteria for PCOS? describe
Rotterdam criteria- need at least 2:
Polycystic ovaries, oligo-ovulation/anovulation, clinical and/or biochemical signs of hyperandrogenism
Investigating PCOS?
Testosterone (normal or high), SHBG (normal or low), LH (high), USS, fasting glucose/oral glucose tolerance test
Management of PCOS?
MDT management, advise on cardiac risks
Weight control and exercise, COC pills or IUS, metformin can be used
Complications of PCOS?
Infertility, endometrial hyperplasia/cancer, CVD, T2DM, sleep apnoea
Abnormal formations of uterus ?
Due to incomplete fusion of mullerian or paramesonephric ducts:
Complete failure (double vagina, cervix and uterus)
Some fusion (single vagina and cervix, double single horned uteruses partially fused)
Septate uterus (midline septum)
Arcuate
Unicornuate
Abnormal formations of vagina?
Vaginal agenesis, vaginal atresia, mullerian aplasia, transverse vaginal septa
Turner syndrome genotype?
45X
What is Asherman syndrome?
How to manage?
Formation of intrauterine adhesions; usually due to injury to endometrium
Tendency to develop them after pregnancy
Mx; lysis of adhesions via hysteroscopy
Presentation of asherman syndrome?
Infertility, loss of pregnancy, menstrual abnormalities, abdominal pain
How might prolactinoma present?
Galactorrhoea, amenorrhoea/oligomenorrhoea, anovulatory cycles, infertility, hirsutism, decreased libido
How to manage prolactinoma?
Dopamine agonists eg cabergoline
Surgery
Oestrogen contraception
What can cause pelvic inflammatory disease?
STIs esp gonorrhoea and chlamydia
Mycoplasmas, flora, strep, TB
Presentation of pelvic inflammatory disease?
Bilateral lower abdominal pain, deep dyspareunia, abnormal bleeding, purulent discharge, may have fever, may have N/V, urinary symptoms, proctitis and adnexal mass
Investigating PID?
STI swabs, pregnancy test, laparoscopy (single best diagnostic test), exclusions eg UTI
How to manage PID?
Analgesia
Abx immediately before swab results- IM ceftriaxone 500mg stat then doxycyline 100mg bd and metronidazole 400mg bd for 14 days
Partner notification and treatment
Recent coil insertion but got PID?
If coil recently inserted can leave in, but if no response to abx in 48-72 hour, remove and prescribe any emergency contraceptives if needed
Complications of PID?
Infertility, ectopic pregnancy, chronic pelvic pain, perihepatitis, tubo-ovarian abscess, reactive arthritis, preterm delivery, vertical transmission
How many stages of labour are there?
3
describe the 1st stage of labour
Cervix dilation.
Early labour:
-Latent phase- cervix starts to soften, irregular contractions=hours-days
-Established labour- cervix dilated to 4cm and regular contractions
-Established labour- dilation 6-10cm
How can you speed up labour?
ARM=artificial rupture of the membranes
or oxytocin drip
Describe the 2nd stage of labour
Full cervix dilation up to birth aka the pushing stage
How long does 2nd stage of labour generally take in primiparous women? Multiparous women?
Primi= less than 3 hours Multi= less than 2 hours
Describe the 3rd stage of labour
Delivery of placenta
Two ways of 3rd stage of labour happening?
Active=oxytocin IM injection
or
Physiological= natural where the cord isn’t cut until it’s stopped pulsing, can take about an hour
Pros and cons of active 3rd stage of labour?
Pros= much faster delivery of placenta and lowers risk of postpartum haemorrhage Cons= increased risk of nausea and can make afterpains worse
What counts as premature labour?
Regular contractions resulting in dilation of cervix after week 20 and before week 37 of pregnancy
Presentation of premature labour?
Contractions, constant low dull back ache, pelvic pressure, mild cramps, spotting or light bleeding, rupture of membranes, change in vaginal discharge
Potential risk factors for premature labour?
Multiple pregnancy, previous preterms, shortened cervix, cigarettes, drugs, infections, chronic conditions, stress, polyhydramnios, foetal birth defect, age of mother
How to try to prevent premature labour?
Regular prenatal care, healthy diet, avoid risky substances, pregnancy spacing, cautious with IVF/how many embryos
How should you manage premature labour?
If unwell, speed up delivery with oxytocin/induction/C-section
If over 34 weeks, then let labour progress naturally
Corticosteroids if between 23 and 34 weeks if risk of delivery in next week
Tocolytics can be used for around 48 hours to buy time for course of steroids/transfer time
Magnesium sulfate venous infusion to reduce risk of cerebral palsy for under 34 weeks
What to give if in labour before 34 weeks gestation?
Magnesium sulfate, steroids
Tocolytics if need to buy time (about 48 hours)
Define premature rupture of membranes (prom)?
Rupture of foetal membranes at least one hour prior to the onset of labour in over 37 weeks gestation pregnancies
How common is premature rupture of membranes?
10-15% term pregnancies
Define preterm premature rupture of membranes (p-prom)
rupture of membranes at least one hour prior to onset of labour in under 37 weeks of gestation pregnancies
Incidence of preterm premature rupture of membranes
Associated with 40% preterm deliveries
What comprises foetal membranes?
chorion and amnion
What can cause premature rupture of membranes?
Early activation of normal physiological processes (enzymes)
Infection (inflammatory markers weaken the membranes)
Genetic predisposition
Risk factors for premature rupture of membranes?
Smoking, previous PROM, vaginal bleeding, lower genital tract infection, invasive procedures eg amniocentesis, polyhydramnios, multiple pregnancy, cervical insufficiency
Presentation of premature rupture of membranes?
“broken waters”- painless popping sensation then gush of watery fluid or non specific eg gradual leakage
Management of suspected premature rupture of membranes?
Speculum exam- pooling in posterior vaginal fornix (need to lie down for at least 30 mins to see this)
Avoid digital vaginal examination until active labour
High vaginal swab- if GBS then start clindamycin/penicillin during labour
Complications of premature rupture of membranes?
Chorioamnionitis, oligohydramnios, neonatal death, placental abruption, umbilical cord prolapse
Commonest associations with placental insufficiency and low birthweight?
DM, htn, clotting disorders, anaemia, medications especially blood thinners, smoking, drug abuse especially cocaine/heroin/methamphetamine, placental poor attachment or placental abruption
Risk of placental insufficiency
- to mum?
- to baby?
Mum= preeclampsia, placental abruption, preterm labour and delivery Baby= greater risk of o2 deprivation, hypothermia, hypoglycaemia, hypocalcaemia, polycythaemia, premature, c-section, stillbirth, death
What is a miscarriage?
2 types?
Loss of pregnancy before 24 weeks gestation
Early miscarriage= more common- 1st trimester (before 12-13 weeks)
Late miscarriage=13-24 weeks
How common is miscarriage?
Very! 20-25% of pregnancies
Risk factors for miscarriage?
Over 30, previous miscarriage, obesity, chromosomal abnormalities, smoking, uterine anomalies, previous uterine surgery, anti-phospholipid syndrome, coagulopathies
Presentation of suspected miscarriage?
Vaginal bleeding, cramping pain, incidental finding on USS
Positive pregnancy test and bleeding +/- pain
Investigations for suspected miscarrage?
Transvaginal USS is 1st line
Serum b-HCG if us not available
Management of miscarriage?
If late miscarriage- need anti- D prophylaxis if rh neg
Conservative/expectant=allow to pass naturally
Medical=vaginal misoprostol (prostaglandin analogue- stimulates cervical ripening and contractions)
Surgery= manual vacuum aspiration if early miscarriage or for evacuation of retained products of conception
Classification of miscarriages?
Threatened, inevitable, missed, incomplete, complete, septic
Describe a threatened miscarriage
Mild bleeding +/- pain, cervix close - still a viable pregnancy
Describe an inevitable miscarriage
Heavy bleeding, clots, pain, cervix open- internal cervical os opened
Foetus viable or non viable
Describe a missed miscarriage
Asx or hx of threatened miscarriage, ongoing discharge, small for dates uterus
Describe an incomplete miscarriage
Products of conception partially expelled, sxs of missed miscarriage or bleeding/clots
Describe a septic miscarriage
Infected POC: fever, rigors, uterine tenderness, bleeding/discharge, pain
Define recurrent miscarriage
At least 3 consecutive pregnancies with miscarriage
What is gestational diabetes?
Any degree of glucose intolerance with onset of first recognition during pregnancy
Why does gestational diabetes occur?
Progressive insulin resistance in pregnancy and insulin requirements rise by 30% during pregnancy
A borderline pancreatic reserve is unable to respond to higher requirements and causes transient hyperglycaemia (insulin resistance falls after pregnancy)
RFs for gestational diabetes?
BMI over 30, asian, previous gestational dm, 1st degree relative with dm, PCOS, previous macrosomic baby (pver 4.5kg)
How would gestational diabetes present? What investigation
Px= asx or DM sxs eg polyuria/dipsia and fatigue
Ix=OGTT
How to manage gestational diabetes?
Lifestyle advice, capillary glucose measurements qds, may need metformin (glibenclamide 2nd line) or insulin
Deliver at 37-38 weeks if on treatment
Stop treatment immediately after delivery then 6-13 weeks later do a fasting glucose test to confirm transience
Foetal complications of gestational diabetes
Macrosomia, organomegaly, erythropoiesis, polyhydramnios, increased rate of pre-term delivery
Neonatal hypoglycaemia
Pathophysiology of pre-eclampsia
Incomplete remodelling of spiral arteries causes a high resistance low flow uteroplacental circulation (the constrictive muscular walls are maintained)
Increased BP, hypoxia and oxidative stress leads to inadequate uteroplacental perfusion causing a systemic inflammatory response and endothelial cell dysfunction
Risk factors for pre-eclampsia? 3 moderate and 3 high
Moderate= nuliparity, over 39 years, BMI at least 35, FH, pregnancy interval over 10 years, multiple pregnancy High= chronic htn, htn/pre-eclampsia/eclampsia in previous pregnancy, CKD, DM, autoimmune diseases
How to do and who to consider prophylaxis for pre-eclampsia?
75mg aspirin/day from 12 weeks to birth
In women with at least 1 high or at least 2 moderate risk factors
Pre-eclampsia potential features
hypertension (2 occasions at least 4 hours apart, over 140/90)
significant proteinuria
over 20 weeks gestation
How does pre-eclampsia present?
Asx, frontal headaches, visual disturbance, epigastric pain, hyperreflexia, sudden onset non-dependent oedema
Classification of pre-eclampsia
Mild= 140/90-149/99
Mod=150/100-159/109
Severe= at least 160/110 and proteinuria or at least 140/90+sxs+proteinuria
Does pre-eclampsia resolve?
Yes, following placental delivery
Management of pre-eclampsia?
Monitoring, VTE prevention, antihypertensives= labetalol (1st line), also nifedipine/methyldopa, delivery!
After delivery, monitor BP for 2 days then once every 3-5 days
Maternal complications of pre-eclampsia?
HELLP syndrome (haemolysis, elevated liver enzymes, low plateletes), eclampsia, aki, dic, ards, htn, stroke, death
What is eclampsia?
Pre-eclampsia and convulsions
Obstetric emergency
Presentation of eclampsia?
Most seizures occur in postnatal period
New onset tonic clonic type seizure, lasting about 60-75 seconds with variable post ictal period
S+Ss relating to end organ dysfunction
Foetal complications of eclampsia?
Intrauterine growth restriction, prematurity, IRDS, foetal death, placental abruption
How to manage eclampsia?
Resuscitation
Seizure cessation with magnesium sulfate
BP control with labetalol and hydralazine
Prompt delivery via C section after mother stabilised
Postpartum and postnatal monitoring and follow up
Why might people with essential hypertension prior to pregnancy not need treatment during their pregnancy?
Physiological drop in BP during pregnancy, so may even get hypotension, or sustain BP below 110/70
What is target BP during pregnancy?
Less than 135/85
How to manage essential hypertension during pregnancy?
Stop ACEi/ARB and start labetalol (1st line)
Nifedipine (2nd line), methyldopa (3rd line)
From 12 weeks onwards 75-150mg aspirin daily
What is placenta praevia? 2 types?
Placenta fully or partially attached to lower uterine segment
Minor= low placenta, but doesn’t cover internal cervical os
Major= placenta lies over internal cervical os
RFs for placenta praevia?
Previous C-section (higher risk with greater number), high parity, age over 40, multiple pregnancy, PMH, endometritis
How does placenta praevia present?
Painless vaginal bleeding
Causes of antenatal haemorrhage?
Placental abruption, placenta praevia, vasa praevia, uterine rupture, local genital causes
How to manage placenta praevia?
ABCDE
If incidental finding at 20 week scan; minor= repeat scan at 36 weeks, major=repeat scan at 32 weeks
C-section=safest mode of delivery (38 weeks for major)
Anti-D within 72 hours of onset of bleeding to Rh neg mother
What is placenta accreta?
Placenta grows too deeply into uterine wall and part/all of placenta remains attached after childbirth- can cause severe haemorrhage
What is placenta percreta?
Placenta grows through the uterine wall
RFs for placenta accreta?
Previous C section, low placental position, maternal age, increased number if pregnancies
Management of placenta accreta?
Confirm on MRI
C-section at 36 weeks and hysterectomy (helps to prevent haemorrhage if there’s an attempt to separate placenta)
What is placenta increta?
Placenta invades into muscles of uterus (form of placenta accreta)
What is placental abruption? Why does it occur?
Part/all of placenta separates from uterine wall prematurely (cause of antenatal haemorrhage)
Due to rupture of maternal vessels within basal layer of endometrium- blood accumulates and splits the placental attachment
2 types of placental abruption?
Revealed- blood drains through the cervix
Concealed- bleeding remains within uterus causing a retroplacental clot
RFs for placental abruption?
PMH (most predictive factor), pre-eclampsia/htn, abnormal lie of baby, polyhydramnios, abdo trauma, smoking, drugs, bleeding in 1st trimester, thrombophilia, multiple pregnancy
Presentation of placental abruption?
Painful bleeding
Management of placental abruption?
ABCDE
Emergency delivery due to maternal and/or foetal compromise
Induction of labour
Conservative
Anti-D if applicable within 72 hours of bleeding onset
How to reduce the risk of a retained placenta?
Use active management in third stage of labour with syntocinon
Presentation of retained placenta?
Fever, badly smelling discharge, heavy bleeding, pain
Management of retained placenta?
Empty bladder/change position
Pull on umbilical cord
Surgery to scrape it away
What is uterine rupture? Two types
Obstetric emergency: Full thickness disruption of uterine muscle and overlying serosa, typically during labour, can extend to affect bladder or broad ligament
Incomplete= intact peritoneum over uterus, uterine contents remain in uterus
Complete= torn peritoneum, uterine contents can escape into peritoneal cavity
RFs for uterine rupture?
Previous C-section/uterine surgery, induction, obstruction of labour, multiple pregnancy, multiparity
Presentation of uterine rupture?
Non specific
Sudden, severe abdo pain persisting between contractions, may have vaginal bleeding
Management of uterine rupture?
ABCDE
Emergency C section and uterus repair or hysterectomy
(decision-incision interval should be less than 30 mins)
What is cervical show?
Small amount of bleeding from vagina caused by rupture of small blood vessels in cervix due to contractions- slow cervical dilatation
Part of labour
What is vasa praevia?
Foetal blood vessels run near/over internal cervical os- likely to rupture in active labour as unprotected by placental tissue or wharton’s jelly of umbilical cord
How does vasa praevia present?
Vaginal bleeding (fresh red blood), rupture of membranes and foetal compromise
How to manage vasa praevia?
Emergency C sections
Improved mortality rates if picked up on USS and using a planned C section
What differentiates antepartum haemorrhage from miscarriage?
Timing
Miscarriage= before 24 weeks
Antepartum haemorrhage= bleeding from birth canal after 24th week of pregnancy until second stage of labour complete
Causes of antepartum haemorrhage?
Major ones= placenta praevia and placental abruption
Also= local causes (infection, trauma, tumours), vasa praevia, uterine rupture, inherited bleeding problems
How to differentiate placenta praevia from placental abruption clinically?
Both=bleeding
Pain=abruption
Painless=praevia
What volume of blood for minor antepartum haemorrhage?
Blood loss less than 50ml and stopped
What constitutes major anterpartum haemorrhage?
50-1000ml blood loss with no signs of shocks
What constitutes massive antepartum haemorrhage?
Over 1000ml blood loss and/or signs of shock
Management of antepartum haemorrhage?
ABCDE
DO NOT attempt vaginal examination
Consider delivery
Urgent USS, foetal monitoring (CTG), anti-D if indicated
Minor and major primary post partum haemorrhages?
Minor= 500-1000ml within 24 hours Major= over 1000ml within 24 hours delivery or signs of shock
Two broad groups of causes of post partum haemorrhage?
Primary and secondary
Primary causes of post partum haemorrhage?
Four Ts= tone (uterine atony, distended bladder), trauma, tissue (retained placenta or clots), thrombin (coagulopathy)
Most common=uterine atony then retained placenta
Secondary causes of post partum haemorrhage?
infection (endometritis) or retained products of conception, subinvolution of placental implantation site, pseudoaneurysms, AV malformation
How to manage post partum haemorrhage?
Resuscitation 2 14/16 G cannulas Crystalloid infusion for minor Blood transfusion for major Catheterise Cross match or O neg If uterine atony is cause- fundal rub, bimanual uterine compression to stimulate contraction, oxytocin, ergometrine, carboprost, misoprostol If medical management not working then surgery Antibiotics for endometritis
What is sheehan’s syndrome?
In women who lose life threatening amount of blood in childbirth or have severely low BP, causes hypoxia which causes pituitary gland damage and subsequent HYPOPITUITARISM
How does sheehan’s syndrome present?
Presents slowly over months/years, but may also have inability to breastfeed
S+Ss: a/oligomenorrhoea, slowed mental function, weight gain, hypothyroid, low bp, low glucose, fatigue, irregular HR, breast shrinkage
Complications of sheehan’s syndrome?
Adrenal crisis, hypotension, unintended wt loss, menstrual irregularities
Management of sheehan’s syndrome?
Lifelong hormone replacement eg corticosteroids, levothyroxine, oestrogen, GH
When do baby blues occur?
During first week after childbirth, last for only a few days
Timing of post-partum depression?
Depressive episode within first 12 months postpartum. Peak incidence during first 2 months
Presentation of post partum depression?
Similar to symptoms of regular depression, negative cognitions about motherhood, anxiety surrounding baby
Management of post partum depression?
Social support and psychological therapies
If not breastfeeding can use SSRI as usual, if breastfeeding need to weigh up risk benefit ratio with patient
Timing of puerperal psychosis?
Can develop rapidly over a few hours and starts within days-weeks of delivery
Who is puerperal psychosis more common in?
Those with bipolar affective disorder or other psychotic illness history.
Those with previous postpartum psychosis have 50% chance of recurrence in next pregnancy
FH links
NB/ can develop in women with no past psychiatric history too
How to manage puerperal psychosis?
Most nee to be treated under MHA
Antipsychotic and/or mood stabiliser
Prognosis of puerperal psychosis?
Good!
Most take 6-12 months to recover fully
Earlier diagnosis and intervention improves prognosis further
Causes of puerperal infection?
Most= staph and strep
Highest risk in non-scheduled C section
What is the leading cause of maternal mortality
VTE in pregnancy (about 1/3 of maternal deaths)
Why is there increased risk of VTE in pregnancy?
Changes in protein levels in clotting cascade- increased fibrinogen and decreased protein S
Changed more pronounced as pregnancy progresses (highest risk is post partum)
RFs for VTE in pregnancy?
Pre-existing RFs: thrombophilia, medical co-morbidities, age over 35, BMI over 30, parity over 3, smoking, varicose veins, paraplegia
Obstetric RFs: multiple pregnancy, pre-eclampsia, c-section, prolonged labour, stillbirth, preterm, PPH
What investigations for VTE in pregnancy?
Bloods, compression duplex USS, ECG, CXR then CTPA or V/Q scan
NB/ d-dimer raised anyway in pregnancy so don’t test this
Management of VTE in pregnancy?
LMWH throughout pregnancy until 6-12 weeks post partum
DON’T use warfarin as teratogenic
Prophylaxis if at least 4 RFs during assessment with LMWH
How would amniotic fluid embolism present?
Acutely- hypoxia, resp arrest, hypotension, foetal distress, seizures, shock, confusion, cardiac arrest, DIC
How is a definitive diagnosis of amniotic fluid embolism made?
On post mortem- foetal squamous cells and debris in pulmonary vasculature
Levels of Hb for anaemia diagnosis in different trimesters?
First: Hb<110g/L
Second/third: Hb<105g/L
Postpartum: Hb<100g/L
Why is anaemia likely in pregnancy?
In pregnancy, plasma volume and RBC mass increase but plasma volume increases disproportionately, so there is a haemodilution effect
When do you screen for anaemia in pregnancy?
Screen at booking visit and at 28 weeks
Need to add in 20-28 week screen for multiple pregnancies
Management of anaemia in pregnancy?
Trial of oral iron (1st line management and diagnostic test)
or folate supplementation
When does rhesus disease of the newborn occur and why?
In rhesus negative mums with rhesus positive foetuses
Mum is sensitised to rh positive blood and then produces antibodies which will come into effect on second exposure
Antibodies cross the placenta and attack the foetal RBCs
How will rhesus disease of the newborn/haemolytic disease of foetus and newborn present?
Haemolytic anaemia, jaundice, may have hypotonia, lack of energy
Symptoms may not develop until a few months of age
What tests can be used to determine if there will be haemolytic disease of foetus?
Kleihauer test (see if foetal blood in maternal circulation) Rosette test (incubate rh neg maternal sample with anti-Rh)
How to prevent/decrease risk of haemolytic disease of newborn?
Anti-D to mum and monitoring
UTI in pregnancy, which abx?
Nitrofurantoin is 1st line, but should be avoided at term: 100mg bd 1/52
2nd line= amoxicillin 500mg tds 1/52 or cefalexin 500mg bd 1/52
What percentage of pregnant women carry GBS?
25%
What can GBS cause? Name of pathogen
S. agalactiae
Can cause GBS disease of newborn, chorioamnioitis, endometritis
How does chorioamniotis present?
Fevers, lower abdo tenderness, foul discharge, tachycardia
How does endometritis present?
Fevers, lower abdo pain, intermenstrual bleeding, foul discharge
How will a neonatal GBS infection present?
Pyrexia, cyanosis, resp difficulties, floppiness
How to prevent poor outcomes in GBS positive women?
IV penicillins throughout labour in women (if GBS positive, UTI by GBS, previous baby with GBS, pyrexia during labour, premature, rupture membranes over 18 hours)
When is management for GBS not indicated?
Elective C-section- as no rupture of membranes
What are the risks of having a gonorrhoea infection during pregnancy?
Perinatal mortality, spontaneous abortion, premature labour, early foetal membrane rupture, vertical transmission causing conjunctivitis in foetus- which if untreated can cause long term blindness and damage
What is cephalopelvic disproportion?
Mismatch between size of foetal head and maternal pelvis causing a difficulty in safe passage through the birth canal
How to classify cephalopelvic disproportion? Examples for each
Absolute CPD=true obstruction- permanent/maternal factors (contracted pelvis, pelvic exostoses, spondylolisthesis, tumours) or temporary/foetal factors (hydrocephalus, macrosomia) Relative CPD (brow/face presentations, occipitoposterior positions, deflexed head)
Most common cause of cephalopelvic disproportion?
Contracted pelvis with average sized infant
Management of cephalopelvic disproportion?
Depends when discovered
May have planned C section
May trial a vaginal delivery
What can cause a hypoactive uterus/uterine inertia?
Premature labour, multiple pregnancy: over distension, psychology, contracted pelvis/malpresentation/deflexed head, full bladder, loaded rectum, hypertensive, anaemia/chronic illness, uterine fibroid
Primary or secondary inertia (after a period of good contraction)
Complications of uterine inertia?
Prolonged labour, distress, increased risk of infection, PPH
Management of uterine inertia?
Empty bladder and bowels, oxytocin, may need C section, can use instrumental delivery if head low enough
Define obstructed labour?
Labour dystocia- baby doesn’t exit pelvis due to being physically blocked despite the uterus contracting normally
Causes of obstructed labour?
cephalopelvic disproportion due to small pelvis/large baby/foetal malpresentation/tight perineum/abnormalities
Complications of obstructed labour?
Foetal anoxia, pressure necrosis, foetal death, vesicovaginal fistula
Management of obstructed labour?
Prevention is key!
Mode of delivery chosen on a case by case basis- episiotomy, ventouse, forceps, symphysiotomy, C section
How can shoulder dystocia occur?
After delivery of head, anterior shoulder becomes impacted on maternal pubic symphysis (more common) or posterior shoulder impacted on sacral promontory
RFs for shoulder dystocia?
Pre-labour RFs: previous event, macrosomia, diabetes, BMI over 30, induction of labour
Intrapartum RFs: prolonged 1st stage of labour, secondary arrest, prolonged 2nd stage, augmentation with oxytocin, assisted vaginal delivery
Ultimate complication of shoulder dystocia?
Other complications
Delay in delivery of foetal shoulders causes hypoxia (proportional to time delay)
Others=tears (3rd and 4th degree), PPH, foetal fracture, brachial plexus injury
Signs of shoulder dystocia?
Failure of restitution (foetus doesn't turn to look to the side) Turtle neck (head retracts back into pelvis and neck no longer visible)
Management of shoulder dystocia?
Stop pushing
Avoid downwards traction on foetal head (risk of brachial plexus injury)
Consider episiotomy
Use manoeuvres: McRoberts (hyperflex maternal hips and stop pushing, 90% success rate), suprapubic pressure (sustained or rocking fashion to apply pressure behind anterior shoulder)
Other 2nd line manoeuvres= internal rotation or posterior arm
What is cord prolapse and types of it?
Umbilical cord descends through cervix with/before presenting part of foetus
Occult (incomplete-with foetus but not beyond)
Overt (complete-lower than presenting part in pelvis)
Why does a prolapsed cord cause foetal hypoxia?
Occlusion of umbilical cord and arterial vasospasm due to cold exposure
RFs for cord prolapse?
Breech presentation, unstable lie, artificial rupture of membranes, polyhydramnios, prematurity, PROM, long cord, multiple pregnancy
How to manage cord prolapse?
Avoid handling of cord to reduce vasospasm, manually elevate the presenting part, encourage into left lateral position, consider tocolysis (stop contraction), emergency C-section/quickest mode of delivery
What is lie of foetus? What are potential lies of the foetus? what’s normal?
Lie=relationship between long axis of foetus and mother
Longitudinal, transverse, oblique
Longitudinal is lie if the right way up!
What is presentation of the foetus? What types?
Presentation= foetal part that first enters the maternal pelvis Cephalic vertex (most common and safest), breech, shoulder, face, brow
What is foetal position? What types?
Position of foetal head as it exits birth canal
Occipito-anterior (ideal), occipito-posterior or occipito-transverse
How to manage abnormal foetal lie?
External cephalic version (ECV) between 36 and 38 weeks to manipulate foetus to a cephalic presentation through maternal abdomen
Who can’t you do ECV in?
Recent APH, ruptured membranes, uterine abnormalities, previous C section
How to manage abnormal foetal position?
90% of malpositions spontaneously rotate as labour progresses
If not, rotation and operative vaginal delivery or C section
How to manage malpresentations?
Brow or shoulder- need C section
Face : if chin anterior can have normal labour, but likely to be prolonged, if chin posterior need C section
Types of breech presentation?
Complete (flexed, cross legged appearance)
Frank (extended- flexed at hip and extended at knee)- most common
Footling (extended at knees)
Management of breech presentation?
About 28% babies breech at 28 weeks but only 3% at term, use USS to confirm diagnosis
ECV, if unsuccessful then C-section (vaginal breech birth can be attempted but requires specific manoeuvres)
Complications of breech presentation?
Cord prolapse, foetal head entrapment, prem rupture of membranes, birth asphyxia, intracranial haemorrhage
Types of instrumental delivery/operative vaginal delivery?
Forceps
Ventouse (silastic cup for occipito-anterior or kiwi cup for any position)
Indications for instrumental delivery?
Inadequate progress, maternal exhaustion, maternal conditions where prolonged exertion should be limited, suspected foetal compromise, any clinical concerns
When should you stop using instrumental delivery?
After 3 contractions and pulls with any instruments with no reasonable progress, should abandon attempt
Pros and cons of ventouse?
Lower success rate, increased foetal injury eg retinal haemorrhage, must be over 34 weeks to attempt
Lower incidence of maternal injuries, less pain
Pros and cons of forceps?
Higher success rate, no maternal effort required
Higher rate of tears
Contraindications to instrumental delivery?
Incomplete dilation, true CPD, breech/face/brow presentation, can’t be under 34 weeks for ventouse
Potential complications of instrumental delivery?
Jaundice, lacerations, haematoma, facial nerve damage, fractures, tears, VTE, incontinence, PPH, shoulder dystocia, infection
What is polyhydramnios?
Amniotic fluid above 95th centile for gestational age
Causes of polyhydramnios?
Idiopathic in 50-60%
Other cases= foetal swallow prevention, duodenal atresia, anaemia, foetal hydrops, twin-twin transfusion syndrome, increased lung secretions, genetic abnormalities, maternal diabetes, maternal lithium ingestion, macrosomia, some TORCH infections
How to diagnose polyhydramnios or oligohydramnios?
On USS using either amniotic fluid index or maximum pool depth
Management of polyhydramnios?
Most don’t need management, good prognosis
May consider amnioreduction or indomethacin (enhances water retention)
What is oligohydramnios?
Low level of amniotic fluid, less than the 5th centile for gestational age
What causes oligohydramnios?
Anything that reduces production of urine, blocks output from foetus, or ruptures the membranes
Main causes= preterm premature rupture of membranes, placental insufficiency, renal agenesis (Potter’s syndrome), non functioning foetal kidneys, obstructive uropathy, genetic/chromosomal anomalies, viral infections
What test to do if considering ruptured membranes as the cause of oligohydramnios?
IGFBP-1 in vagina (bedside test)
How to manage oligohydramnios?
Manage underlying cause
Ruptured membranes- labour likely to commence within 24-48 hours, consider induction, need steroids and abx
Placental insufficiency- likely to be delivered before 36/37 weeks
Prognosis of oligohydramnios in 2nd trimester?
Poor
Decreased amniotic fluid means decreased foetal movements, which causes muscle contractures
Pathophysiology of pubic symphysial dysfunction?
Physiological pelvic ligament relaxation and increased joint mobility in pregnancy causes discomfort and pain in pelvic area, may radiate to upper thighs and perineum
Joint sufficiently relaxed to allow instability in pelvic girdle- excessive movement of pubic symphysis in anterior or lateral direction
What other factors apart from pregnancy itself can contribute to pubic symphysial dysfunction?
Strenuous work during pregnancy, weight gain, multiparity, increasing age, history of difficult deliveries
Presentation of pubic symphysial dysfunction?
PAIN- variable, usually relieved by rest, disappears commonly after giving birth
LOCOMOTOR difficulties- walking, stairs, chairs, weight bearing activities, turning in bed, standing on one leg
How to manage pubic symphysial dysfunction?
Analgesia (paracetamol) then after delivery can use NSAIDs
Weight-bearing aids, physio and exercise
Most common cause of intrauterine growth restriction? Consequences of IUGR?
Placental insufficiency
Consequences: lack of oxygen at birth, premature labour, hypoglycaemia, hypocalcaemia, stillbirth, increased RBC
When is booking appointment and what happens there?
8-12 weeks
Provide info, decide care plan, BP, BMI, urine, identify any risks, screen for vulnerabilities
When do multiparous women have appointments in antenatal schedule?
GP contact, 8-12 week booking and 8-14 week dating scan
16 weeks, 20 week anomaly scan, 28 weeks, 34 weeks, 36 weeks, 38 weeks
What extra appointments do nulliparous women get in antenatal schedule?
25 weeks, 31 weeks, 40 weeks
What sorts of things are done in antenatal schedule?
(Sickle cell/thalassaemia screening offered before 10 weeks)
BP, urine, screening, measure uterus, care plan, any anti-D injections, information giving, checking position of foetus, ECV if required
What may be discussed at 41 week appointment?
Offer a membrane sweep, discuss induction
What is looked at in the 20 week/anomaly scan?
Looks at bones, heart, brain, spinal cord, face, kidneys, abdomen and can determine sex
What 11 conditions does the 20 week scan look for?
Anencephaly, open spina bifida, cleft lip, diaphragmatic hernia, gastroschisis, exophthalmos, serious cardiac abnormalities, bilateral renal agenesis, lethal skeletal dysplasia, Edward’s syndrome (trisomy 18), Patau’s syndrome (trisomy 13)
How are the trisomies screened for?
Combined test (USS and blood test) then nuchal translucency measurement at 12 week scan
For trisomy 21, can do quadruple blood screening test iif combined not done- done at 14-20 weeks
At what point is routine anti-D prophylaxis given?
28 and 34 weeks
Different types of breast cancer?
Ductal carcinoma in situ, invasive lobular carcinoma, angiosarcoma, inflammatory breast cancer, lobular carcinoma in situ, male breast cancer, Paget’s disease of the breast, recurrent breast cancer
How will breast cancer present?
Lump/thickening, change in size/shape/appearance, skin changes, newly inverted nipple, peeling/scaling/crusting of areola or breast, redness or pitting
RFs for breast cancer?
BRCA1/2, female, increasing age, history of breast condition, previous breast cancer, family history, genes, radiation exposure, obesity, puberty under 12, menopause over 55, first child at older age, nulliparous, postmenopausal HRT, alcohol
What is involved in triple assessment of breast cancer?
Breast examination
Mammogram/USS
Biopsy
How is breast cancer managed?
Depends on stage and prognosis
Surgery (lumpectomy, mastectomy, sentinel node biopsy, axillary LN dissection, prophylactic mastectomy)
Radiation, chemo, hormone therapy
What hormone therapies may be used in breast cancer?
Selective oestrogen receptor modulators/SERMs eg tamoxifen
Aromatase inhibitors eg anastrozole
Surgery/medication to suppress ovaries
When is breast screening undertaken?
Every 3 years between 50 and 70 years
When are implants allowed on the NHS?
Severe asymmetry or amastia
2 types of breast implants with pros/cons
Silicone- most common, less likely to rupture, more natural, can spread into breast and cause lumps
Saline- more likely to fold/rupture/go down over time, but will be absorbed safely into the body
What is the earliest form of breast cancer?
In situ carcinoma- abnormal cells inside milk duct
Presentation of paget’s disease of the nipple
Flaky/scaly nipple, crusting/oozing/hardened skin, itch, erythema, tingling/burning sensation, inverted/flattened nipple, lump
Usually unilateral
3 common benign breast lumps?
Breast abscess, cysts, fibroadenoma (most common)
Two kinds of breast abscess?
Lactational-peripheral region of breast, commonly upper and outer quadrant
Non lactational-central/subareolar or lower quadrants
Risk factors for breast abscess?
Previous mastitis, immunosuppressed, S. aureus carriage, poor hygiene
How will breast abscesses present?
Recent history mastitis or previous abscess, fever, general malaise, painful swollen lump, inflammatory signs
Lump may be fluctuant with skin discolouration
How to manage breast abscess?
Diagnose by USS.
Drainage then culture fluid to guide abx choice, advise lactating women to continue breastfeeding
How do breast cysts present?
Smooth and mobile, round/oval lump
May have nipple discharge (clear/yellow/brown)
Pain/tenderness over area
Increased size/tenderness just before period
Symptoms improve after period
Do breast cysts require treatment?
Generally no
Different types of fibroadenoma?
Simple, complex, juvenile, giant (over 2 inches), phyllodes tumour (risk of becoming malignant)
How does a fibroadenoma present?
Most often in 15-35 year olds
Round, distinct smooth borders, easily moved, firm or rubbery, painless lump
Lumps can become bigger during pregnancy/use of hormone therapy, might shrink after menopause
What swabs in double swab? Triple swab?
Double= NAAT then high vaginal charcoal media Triple= NAAT, then high vaginal charcoal media and endocervical charcoal media swab
What does NAAT swab detect for? Where to swab?
Swab endocervical or vulvovaginal
Detects chlamydia and gonorrhoea
What does a charcoal media swab detect? Where to swab?
High vaginal swab
Detects BV, trichomonas vaginalis, candida, GBS
RFs for vulvovaginal candidiasis?
Pregnancy, diabetes, broad spectrum abx, corticosteroids, immunocompromised
How does thrush present?
Pruritus vulvae, discharge (white, curd like, non offensive), dysuria (superficial), erythema and swelling of vulva, satellite lesions (red, pustular with superficial white/creamy pseudomembranous plaques that can be scraped off)
How to manage thrush?
No need to investigate if uncomplicated
Initial pessary antifungal eg clotrimazole (pregnancy= only option, don’t use oral)
Consider oral antifungal eg fluconazole
Topicla imidazole in conjunction to address vulval symptoms
If symptoms persisting over 7-14 days, need to review
If recurrent/ complicated- need vaginal smear and microscopy
Organism causing chlamydia? Incubation period?
Chlamydia trachomatis (bacterium). 7-21 days incubation
Presentation of chlamydia?
70% women asymptomatic, 50% men asx
Dysuria, abnormal discharge, intermenstrual/postcoital bleeding, dyspareunia, lower abdo pain, cervicitis +/- contact bleeding, mucopurulent endocervical discharge, pelvic tenderness, cervical excitation
Investigations for chlamydia?
National screening for sexually active under 25s
Vulvovaginal swab then for NAAT (endocervical swab or 1st urine catch are 2nd line alternatives)
How to manage chlamydia?
Doxycyline orally 100mg bd for 1 week
or
stat azithromycin 1g
Avoid sex until treatment completed, partner tracing
How does bacterial vaginosis present?
50% asx, offensive fishy smelling discharge, not usually associated with irritation
Thin, white grey discharge. Increased vaginal pH
Pathophysiology of BV?
some disturbance in natural vaginal flora, causes a decrease in lactobacilli. This increases the pH and allows a polymicrobial infection- especially Gardnerella vaginalis, anaerobes and mycoplasma
RFs for BV?
sex, IUD, receptive oral sex, STI present, douching, recent abx, smoking, black
Investigating for BV?
High vaginal smear and microscopy
Can do vaginal pH over 4.5
Can do KOH whiff test (alkali added causing strong fishy odour)
Management for BV?
oral metronidazole 400mg bd for 5-7 days or stat 2g
Can use topical gel
What causes trichomoniasis?
Curable STI by protozoan Trichomonas vaginalis
Presentation of trichomoniasis?
Commonly asx, offensive vaginal odour, abnormal discharge (yellow-green), vulval irritation, dyspareunia, dysuria, vulvitis, strawberry cervix
Management of trichomoniasis?
Metronidazole- 2g stat or 400-500mg bd for 5-7days
Partner trace (preceding 4 weeks)
Abstain from sex until treatment completed
Cause of gonorrhoea?
Neisseria gonorrhoea (bacteria)
Presentation of gonorrhoea?
Around 50% asx, sxs occru 2-5 days after infection, altered/increased discharge (thin, watery, green or yellow), dysuria, dyspareunia, lower abdo pain, rarely causes unexpected bleeding
Often co-exists with chlamydia infection
Management of gonorrhoea?
IM ceftriaxone 1g and partner notification
Which herpes causes what?
HSV-1= genital herpes and cold sores HSV-2= genital herpes
How will a primary HSV infection present?
Small red blisters- very painful and can form open sores, discharge, flu like symptoms, itchy genitals
After 20 days lesions crust and heal
How will secondary HSV infections present?
Recurrent outbreaks (shorter and less severe over time), burning and itching, red blisters
How long do cold sores last?
7-10 days
How to investigate and manage HSV infection?
Ix= swab open sore and send for PCR Mx= aciclovir and full STI screen
What causes syphilis?
STI caused by spirochete gram negative bacteria Treponema pallidum
Presentation of primary syphilis?
Bacteria divide forming infectious hard ulcer= chancre forming after 2-3 weeks
Papule>chancre (painless)
Heal within 3-10 weeks, can persist during secondary syphilis
NB/ if chancre left untreated, systemic damage via obliterating arteritis causes ischaemia and symptoms
How does secondary syphilis present?
3 months post initial infection Skin rash (hands and feet), fever, malaise, arthralgia, wt loss, headaches, condylomata lata, painless lymphadenopathy, silver mucous membrane lesion
How does tertiary syphilis present?
Gummatous (non infectious, various tissues)
Neurosyphilis (tabes dorsalis, dementia, meningovascular complications, argyll robertson pupil)
Cardiovascular (aortic regurgitation, angina, calcification of ascending aorta)
How to investigate syphilis?
Dark ground microscopy, PCR, serology, LP (?neuro)
How to manage syphilis?
Penicillin (benzathine)
What may happen 24 hours after treatment of syphilis?
Jarisch Herxheimer reaction- flu like illness
Needs follow up serology
What causes genital warts?
Human papillomavirus (mainly HPV 6 and 11) Needs skin-skin contact
How to manage genital warts?
May not need tx
Topical tx eg podophyllotoxin/imiquimod
Physical ablation (excision, cryotherapy, electrosurgery, laser surgery)
Vaccination!
Describe progression of HIV to AIDS
Single stranded RNA retrovirus uses CD4 cells
Seroconversion (producing anti-HIV abs), flu like illness with decreasing CD4 levels- highly infectious
Latent phase- decreasing Cd4 and increasing viral load
May be asx latent phase initially, then late latent= infectious
Over 10 years or so, becomes AIDS when CD4 is under 200
What investigations for HIV/AIDS?
4th generation tests- HIV antibodies and p24 antigen
How to manage HIV?
HAART reduces viral load to undectable (=untransmissable) levels, but not a cure- atripla, eviplera etc
PEP if within 72 hours of contact and taken for a month (truvada and raltegravir)
Pregnant woman with HIV- what to do and what does t reduce risk of transmission to?
Antenatal HAART, avoid breastfeeding, neonate PEP
Reduced risk from over 25% to less than 1%
4 phases of sexual arousal?
Excitement, plateau, orgasmic, resolution
What happens in excitement phase in men?
Psychogenic or somatogenic stimuli
Sacral parasympathetic
Arteriolar vasodilation in corpora cavernosa, penile filling (latency) and penile tumescence (erection)
What happens in plateau phase in men?
Sacrospinous reflex
Contraction of ischiocavernosus, venous engorgement and decreased arterial inflow, testes engorged and elevated
Secretion from accessory glands (5% ejaculate), lubricates distal urethra and neutralises acidic urine
Increased HR and BP
What happens in orgasmic phase in men?
Emission= thoracolumbar sympathetic reflex- contraction of smooth muscle, internal and external urethral sphincters contract, semen pools in urethral bulb (mixing of ejaculate contents) Ejaculation= spinal reflex (l1, l2), contraction of glands and ducts and urethral sphincter, filling internal urethra stimulates pudendal nerve- contracts genital organs and expels semen
What happens in resolution phase in men?
Thoracolumbar sympathetic- contraction of arteriolar smooth muscle, increased venous return, causes dehumescence flaccidity and refractory period
Nervous system control of female 4 phases of sexual arousal?
Excitement= sacral parasympathetic Plateau= sacrospinous reflex Orgasmic= thoracolumbar sympathetic reflex and spinal reflex Resolution= thoracolumbar sympathetic
Describe excitement phase in women?
Vasocongestion, vaginal lubrication, clitoris engorges, uterus elevates, increased muscle tone/HR/BP, inner 2/3 of vagina lengthens and expands
Describe plateau phase in women?
Increased tone/HR/BP, labia minora deepends in colour, clitoris withdraws under hood, bartholin glands secretion to lubricate vestibule, uterus completely elevated and orgasmic platform forms in lower 1/3 of vagina
Describe orgasmic phase in women?
Orgasmic platform contracts rhythmically 3-15 times, uterus and sphincter contracts
Describe resolution phase in women?
Clitoris descends, labia return to normal size and colour, uterus descends, vagina shortens and narrows, no refractory period
What happens to aid the sperm to reach the ampulla for fertilisation?
Oxytocin stimulates uterus to contract aiding travel
Sperm undergoes capacitation- tail movement changes from beat like action to thrashing whip like action, also removal of protein coat of sperm exposes the acrosome enzymes which allows penetration of zona pellucida
Physiology of sperm fertilising the ovum
After capacitation, zona pellucida 3 (ZP3) proteins interact with sperm and allow calcium to enter spermatozoa, causing increased cAMP
Acrosome swells, outer membrane fuses with sperm plasma membrane- releases enzymes
Inner cell membrane of acrosome exposed, ZP2 glycoprotein holds sperm near egg
Proteolytic enzymes penetrate ZP and sperm and oocyte membranes fuse and calcium enters cells stopping them moving
What prevents polyspermy?
Calcium enters, egg cell membrane depolarises (primary block preventing polyspermy)
Cortical reaction where granules in egg release contents into ZP (secondary block to polyspermy)
Final meiotic division (polar body released)
How does the placenta form?
Formed form outer trophoblast cells
Day 9- lacunae/spaces form within syncytiotrophoblast and this erodes maternal tissues allowing maternal blood from uterine spiral arteries to enter the lacunar network
Cytotrophoblast forms primary chorionic villi which penetrate and expand into syncytiotrophoblast, by 3rd week secondary chorionic villi form
Villi expand into branching villi to form surface area for exchange
How does the placenta change throughout trimesters?
First= thick placental barrier
By full term= increased surface area but barrier much thinner and cytotrophoblast layer is lost from first trimester
What is the placenta covered by on maternal and foetal side?
Maternal= decidua basalis Foetal= chorionic plate
at 4/5th month, what happens to placenta?
Decidua form decidual septa- divides placenta into cotyledons, where each receives blood supply from 80-100 spiral arteries
What does the placenta like by full term?
Discoid, 15-25 cm diameter, 3cm thick, weighs about 500g
Maternal side has about 15-20 bulging areas
What score can be used to judge likelihood of woman entering labour soon?
Bishop scoring
What factors are considered in bishop scoring?
Dilation, effacement (how thin cervix is), consistency (should be a soft cervix), position (cervix should move forward with head), foetal station (how far up baby’s head is)
What different bishop scores mean?
Over 8= spontaneous labour about to start soon
6 or 7= unlikely to start soon, induction of labour could go either way
Under 5= unlikely and induction probably won’t work
What is a partogram?
Document used to monitor labour
Records maternal obs, foetal HR, amniotic fluid, contraction frequency and strength, position, cervicograph, any oxytocin administration, urine, all vaginal examinations
What does cardiotocography measure?
Foetal HR and contractions
How can CTG be performed?
External maternal elastic belt
Can insert vaginal electrode for FHR
Indications for CTG?
Premature/smaller than expected, htn, fever, infection, fresh blood passed in labour, multiple pregnancy, passed meconium, premature rupture of membranes, unusual foetal position, labour sped up or epidural needed
What are foetal scalp samples?
Used during labour to confirm foetal oxygenation
Create shallow cut by a transvaginally inserted blood lancet
Tests pH and lactate as acidosis a/w hypoxia
When would you do a foetal scalp sample?
If CTG suggested pathology
Indications for amniocentesis?
Genetic testing eg trisomy 21
Foetal lung testing- if mature enough for birth (32-39 weeks)
Diagnosis of foetal infection
Evaluate severity of anaemia in babies with Rh sensitisation
Polyhydramnios treatment
Paternity testing
When is genetic amniocentesis performed?
Between 15-20 weeks
Risks of amniocentesis?
Leaking amniotic fluid, miscarriage, needle injury, Rh sensitisation, infection, infection transmission
When is chorionic villus sampling done?
Usually between 11-14 weeks, but can be done as early as 10 weeks
What can chorionic villus sampling not detect?
Neural tube defects (but genetic amniocentesis can)
Cons of chorionic villus sampling?
Risks of miscarriage, rh sensitisation and uterine infection
Sometimes results are unclear and may need amniocentesis as well
Rare chance of false positive
What is viability re ejaculate, and the usual number?
What percentage of live sperm are in a semen sample
Should be at least 58%
Examples of fertility medications?
Clomifene (encourages ovulation in women who ovulate irregularly)
Tamoxifen (alternative to clomifene)
Metformin (if has PCOS)
Gonadotrophins
GnRH and dopamine agonists (encourgae ovulation)
Options for assisted conception?
Fertility medications Fertility surgery (fallopian tubes if blocked or scarred, laparoscopy for endometriosis) Intrauterine/artificial insemination In vitro fertilisation Donation (egg or sperm)
Causes of male infertility?
Low sperm production, abnormal sperm function, blockages
Medical eg varicocele, infection, retrograde ejaculation, antibodies, tumours, undescended testes, hormones, tubule defects, chromosome, sex problems, Coeliac, medications, prior surgery
Environmental eg industrial chemicals, heavy metal, radiation, overheated testes
Lifesyle eg drug abuse (anabolic steroids, cocaine, weed), alcohol, smoking, obesity
What is the apgar score?
Describes condition of newborn infant immediately after birth done at 1 minute and 5 minutes
Activity (tone), pulse, grimace (reflex irritability), appearance (colour), respiratory
What apgar score means hypoxia-ischaemia is unlikely?
Over 7 at 5 minutes
2 types of HRT? 2 regimes?
Combined or oestrogen only (for hysterectomy patients)
Regimes= cyclical or continuous
SEs of HRT?
Oestrogen and progestogen related= bloating, breast tenderness, nausea, cramps, headaches, vaginal bleeding
Progestogen related= mood swings, depression, acne, abdo pain, back pain
What defines heavy menstrual bleeding?
Subjectively (what the woman deems) heavy
Causes of menorrhagia?
Most due to a combination of coagulopathy, ovulatory and endometrial dysfunction
Pathological causes=uterine fibroids (20-30%), polyps (5-10%), endometriosis
40-60% women= dysfunctional uterine bleeding
NICE investigation for menorrhagia?
FBC +/- haematinics, coagulation, TFT, TVUS, hysteroscopy +/- endometrial biopsy
Management options for menorrhagia/abnormal uterine bleeding?
1= IUS (Mirena) 2= antifibrinolytics eg transexamic acid 3= NSAIDs eg mefenamic acid 4= progestogens eg medroxyprogesterone acetate or northesisterone 5= COCP 6= POP 7= danazol 8= reassurance 9= endometrial ablation 10= hysterectomy 11= uterine artery embolisation 12= myomectomy/resection fibroids
Example of antifibrinolytic and administration? how does it work?
Transexamic acid 1g TDS for up to 4 days
Inhibits tissue plasminogen activator
How does mefenamic acid work? administration?
inhibits COX and blocks PGE2 receptors
500mg tds until bleeding stops/reduces
When are progestogens least effective in AUB? When must you use them? How long to take them for? 2 examples?
Least effective if in luteal phase. Should use from day 5-25. Take for minimum 3 months
Medroxyprogesterone acetate and northesisterone
How does danazol work?
Inhibits sex steroid production and blocks receptors
Indications for endometrial ablation?
HMB, not expecting amenorrhoea, normal endometrium, uterus under 12 weeks size, completed family
Contraindications to endometrial ablation?
Malignancy, acute PID, desire for future pregnancy, excessive uterine cavity length
Which options for AUB are fertility sparing?
Uterine artery embolisation and myomectomy/resection of fibroid
What time period= puerperium?
From delivery of placenta to 6 weeks following the birth
During involution of uterus and genital tract in puerperium, what different lochia are shed?
Lochia rubra (day 0-4), lochia serosa (day 4-10), lochia alba (day 10-28)
Describe prolactin response in breast feeding?
Baby suckles, sensory impulses from nipple to brain, prolactin from anterior pituitary via bloodstream to breasts, makes lactocytes produce milk
More secreted at night, suppresses ovulation, level peaks after feed (to produce milk for next feed)
Describe oxytocin reflex in breast feeding?
Baby suckles, sensory impulse from nipple to brain, oxytocin released from posterior pituitary, causes myoepithelial cells to contract and expel milk
Helped by sight, sound and smell of baby, hindered by anxiety/stress/pain
Benefits of breastfeeding?
Decreases GI disease, resp disease, otitis media and NEC in baby
Lactoferrin: regulated iron absorption and delivery, boosts immune system
How does post dural puncture headache present?
Headache worse on sitting/standing, starts 1-7 days after spinal/epidural. Neck stiffness, photophobia
RFs for urinary retention in puerperium?
Epidural analgesia, prolonged 2nd stage of labour, forceps/ventouse, extensive perineal lacerations, poor labour bladder care
What is obstetric cholestasis?
Itching with no rash, abnormal liver function (increased AST, ALT and bile acid), resolves after delivery
How to manage obstetric cholestasis?
Urseodeoxycholic acid
Anti-thyroid drug to use in pregnancy?
Propylthiouracil
When would you offer sickle cell and thalassaemia screening?
By 8-10 weeks in all pregnant women
Unbooked women in labour
When are babies to hepatitis B woman vaccinated?
Within 24 hours of birth
4,8,12 and 16 weeks
Then at 12 months
When is the combined test offered?
11+2 to 14+1 weeks
What is involved in the combined test?
Uses maternal age, crown rump, nuchal translucency, 2 biochem markers= PAPP-A and free BHCG
What can combined test screen for?
2 risk results produced
1 for T21
1 for T18/T13
What is quadruple testing for? When to offer?
T21
14+2 to 20+0 weeks or when head circumference is 101-172mm
What is involved in quadruple testing?
Alpha fetoprotein, total BHCG, oestriol and inhibin A
When is the early pregnancy scan done, what for?
10-14 weeks
For dating and confirming viability, can form part of combined test
When is foetal anomaly screening done?
18-20 week
What does the foetal anomaly screening scan look for?
Open spina bifida, anencephaly, cleft lip, diaphragmatic hernia, gastroschisis, exomphalos, serious cardiac abnormalities, bilateral renal agenesis, lethal skeletal dsyplasia, trisomy 13+18
When might transdermal patch HRT be used?
Gastric upset eg Crohns, need for steady absorption (eg migraines), perceived increased risk of VTE, older women, medical conditions eg htn, patient choice
How to diagnose premature ovarian insufficiency?
In under 40
FSH over 25 IU/L in 2 samples 4 weeks apart and 4 months of amenorrhoea
How fertile are you generally around menopause?
For 2yrs if menopause under 50 years
For 1 year if menopause over 50 years
Contraindications to HRT?
Undiagnosed abnormal PV loss, breast lump, acute liver disease
When should you use HRT with caution?
Fibroids, uncontrolled BP, migraine, epilepsy, endometriosis, FH VTE, over 60s
Genes associated with breast cancer?
BRCA1/2, Tp53, PTEN, STKII, CDHI
How to investigate a breast presentation?
Triple assessment: clinical exam, imaging, biopsy.
Everything scored 1-5.
What is the nottingham prognostic index used for?
Formula?
Prognosis of breast cancer if no treatment other than surgery used
Grade (1-3) x nodes (1-3) + 0.2(size cm)
Score 2-7 with 7 being worst prognosis
Receptors used in prognosis and treatment in breast cancer?
ER (positive= good)
PgR (positive=good)
Her2 (positive=bad)
Ki67 (positive=bad)
Endocrine treatment options for breast cancer?
Direct oestrogen receptor inhibitor (pre menopausal)= tamoxifen
Aromatase inhibitors (stops androgen conversion to oestrogen) (post menopausal)= anastrazole, letrozole
Adjuvants for breast cancer therapy?
Chemo, endocrine, trastuzumab/herceptin and pertuzumab (for Her2 +ve), radio, bisphophonates (decrease mets)
What is non cyclical breast pain usually due to`?
Pulled pectoral or serratus muscle
RARELY due to cancer
When can you carry out termination of pregnancy?
Before 24 weeks
After 24 weeks if risk to life of baby or if to prevent grave permanent injury to maternal physical/mental health, or if continuation of pregnancy would involve risks to life of pregnant woman
2 consultants need to sign
Female genital mutilation type 1?
Clitoridectomy (partial or total)
FGM type II?
Excision: clitoris and labia minora (partial or total)
FGM type III?
Infibulation: narrowing of vaginal orifice with creation of a covering seal +/- clitoral excision
FGM type IV?
All other harmful procedures including pricking, piercing, incising, scraping and cauterisation
UK law on FGM?
Offence to perform, assist in carrying out, assist non UK person to carry out FGM outside of UK on UK national or permanent UK resident
Hormones involved in labour?
Prostaglandins, oxytocin, oestrogen (surge at labour to inhibit progesterone to prepare smooth muscle), beta endorphins (natural pain relief), adrenaline (released as birth is imminent), prolactin
What is the most common pelvis type in females? other types?
Gynaecoid most common
others= platypelloid, android, anthropoid
Mechanism of labour?
Descent, flexion of neck, internal rotation, extension, external rotation (naturally aligns head with shoulders), delivery of body (anterior then posterior shoulder)
How much amniotic fluid at term?
500-800mls
What is the term used for when foetus born in intact amniotic sac?
en caul
Why do we allow at least 1 minute before clamping the umbilical cord?
Allows time to transfuse blood to baby (can received up to 214g of blood), allows baby transition time to extra uterine life, increases rbcs/iron/stem cells, decreased need for inotropic support
Analgesia options in labour?
Holistic and non invasive eg aromatherapy, water immersion, massage, TENS
Etonox (gas and air), paracetamol and codeine
Opioids: diamorphine, pethidine, remifentanyl
Epidural (mix of bupivacaine and fentanyl)
2 planes for mammogram?
Craniocaudal (horizontal plates)- for medial breast and deeper parts
Medio-lateral oblique- good for axillary tail and lateral breast
How much does breast cancer screening reduce mortality?
Between 16 and 29%
Main two types of invasive breast cancer?
ductal (70%)
lobular (10%)- harder to feel, more diffuse, more prone to be bilateral
On breast screening, what are ductal carcinomas in situ and how do they look on mammogram?
Pre-malignant, not yet able to invade basement membrane so can’t metastasise
Appear as microcalcifications generally
Fluid and renal physiological changes in pregnancy?
Increased total plasma volume (30-50%)
Favour sodium retention and increase potassium absorption
Increased extracellular fluid; dilution effects
Decreased plasma osmolality without diuresis, decreased plasma oncotic pressure
Increase kidney size (20%)
Dilation of renal system, decreased ureteral tone
Increased renal blood flow, increased GFR
Increased renin-angiotensin II
CV physiological changes in pregnancy?
Peripheral vasodilation early on, increased SV, HR, and CO
BP changes biphasic: early on drop in BP, increase in late pregnancy
Dilution anaemia, increased polymorphs
Hypercoagulable
Resp physiological changes in pregnancy?
Diaphragmatic elevation
Increased maternal oxygen consumption
TLC, FRC, VC and ERV+IRV reduced
Increased TV increases minute volume
Maternal RBCs have increased 2,3 diphosphogylcerate (DPG)- allows o2 release at same po2
GI physiological changes in pregnancy?
Progesterone induced generalised smooth muscle relaxation
decreased CCK and decreased gallbladder motility
Increased gut transit time
Metabolic physiological changes in pregnancy?
Weight gain (mean around 12.5kg) Early= maternal glycogen synthesis and fat deposition, late= maternal insulin resistance
Which pessary will still allow sexual intercourse?
Ring
Different types of hypertension to experience in pregnancy?
Gestational hypertension
Pre-eclampsia, eclampsia
Chronic hypertension
Pre-eclampsia superimposed upon chronic hypertension
What defines gestational hypertension?
New hypertension after 20 weeks gestation
Systolic over 140 and or diastolic over 90mmHg
No or little proteinuria
What counts as chronic hypertension with superimposed pre-eclampsia?
New onset proteinuria after 20weeks or before if there’s a sudden increase in proteinuria/BP, thrombocytopenia or abnormal AST/ALT
What protein:creatinine ratio can be seen in pre-eclampsia?
Over 30mg/mmol
What warrants severe pre-eclampsia?
BP over 160 systolic or 110 diastolic Proteinuria over 5g or +++ on dipstick Oliguria under 400ml in 24 hours CNS signs Pulmonary oedema Epigastric/RUQ pain Impaired LFTs Thrombocytopenia IUGR Oligohydramnios
Definitive cure for pre-eclampsia?
Delivery of placenta
Low birth weight? Very low birth weight? Extremely low birth weight?
Low= under 2500g
Very low= under 1500g
Extremely low= under 1000g
Primary prevention methods for preventing preterm birth?
Smoking cessation, STI prevention, prevent multiple pregnancy (IVF caution), variable work schedules, physical and sexual activity advice, cervical assessment at 20-26 weeks
Secondary prevention methods for preventing preterm birth?
Transvaginal cervical ultrasound, qualitative foetal fibronectin test
Screen high risk asymptomatic women
Manage women with threatened preterm labour with a cervix under 3cm dilated- administer progesterone (pessary), cervical cerclage can be used
How can you manage a woman with threatened preterm birth?
Intravaginal progesterone first line
Cervical cerclage can be used
Tertiary prevention methods for preventing preterm birth?
Prompt diagnosis, tocolysis and antibiotics, corticosteroids
What is foetal fibronectin? significance of it?
Extracellular matrix protein found in choriodecidual interface
Abnormal finding in cervicovaginal fluid after 20 weeks so may indicate disruption of attachment of membranes to decidua
Reappears close to term as labour approaches
What test to look for foetal fibronectin/ FDC-6? downfalls?
ELISA
NB/ false positives eg cervical manipulation, sexual intercourse, lubricants, bleeding
How far away must placenta be from internal cervical os to be considered normal?
At least 20mm
General management for any worrying APH?
ABCDE 2 14/16 G cannulas IV fluids (crystalloid) Cross match 6 units Inform senior colleagues and paediatrics Examination (avoid digital exam) Foetal monitoring +/- delivery Steroids if under 34 weeks
Complications of antepartum haemorrhage?
Premature labour/delivery, blood transfusion, acute tubular necrosis (+/- renal failure), DIC, PPH, ITU admission, ARDS (secondary to transfusion), foetal morbidity and mortality
Uterotonic options?
Oxytocine, ergometrine, carboprost, misoprostol, tranexamic acid
Sepsis 6?
Give three, take three
oxygen, IV abx, IV fluids
Blood cultures, bloods (hb/lactate/glucose), measure hourly urine output
Describe the follicular phase of the menstrual cycle?
Low oestrogen and progesterone
Increasing levels of FSH
Developing follicles release oestrogen
This inhibits FSH and leads to one dominant follicle
Oestrogen levels rise high enough to induce positive feedback on pituitary (not negative)
LH surge= ovulation
Describe the luteal phase of the menstrual cycle?
Follicle forms corpus luteum which secretes progesterone
Progesterone peaks 7 days after ovulation and unless maintained by the pregnancy, corpus luteum regresses to corpus albicans
Falling progesterone induces menstruation
When does progesterone level peak in menstrual cycle?
7 days after ovulation
eg day 21 in 28 day cycle
eg day 28 in 35 day cycle
How many days from ovulation to menstruation?
14 days
What maintains the corpus luteum in pregnancy?
HCG secreted by synctiotrophoblast (similar to FSH and LH)
Continues to secrete progesterone until the placenta takes over at about 12 weeks
How does the COCP work?
provides a constant level of oestrogen and progestogen, causes negative feedback on FSH and LH
This prevents development of follicles and stops the LH surge so no ovulation!
In fertility investigations, when to check baseline FSH and LH?
Day 2-5
What happens in the menstrual phase of the menstrual cycle?
Falling levels of progesterone cause shedding of the endometrium; spasm of spiral arterioles, ischaemic necrosis and generalised inflammation
What happens in the proliferative phase of the menstrual cycle?
Endometrium grows under the influence of oestrogen. Early development of glands and spiral arterioles
What happens in the secretory phase of the menstrual cycle?
After ovulation, progesterone dominates
Development of complex glands, increase in spiral arterioles, endometrial cells produce and store glycogen
Endometrium stops growing so much but prepares for implantation
Why do obese people produce more oestrogen?
Increased aromatase
How do progestogen contraceptives work?
Maintain the thin uterine lining and inhibit action of oestrogen- stops menstruation by avoiding the drop in progesterone before menstruation
What is cervical motion tenderness or cervical excitation seen in?
PID and ectopic pregnancy
What is pelvic congestion syndrome?
Incompetence of pelvic vein valves, typically occurring after pregnancy
Causes constant dull lower abdo ache which is worse after standing/exercise
How to investigate pelvic congestion syndrome? How to manage?
Transvaginal duplex USS or MRI venogram
Mx= analgesia, or non invasive transcatheter vein embolisation
What is sampson’s theory?
Retrograde menstruation contributing to endometriosis
