O&G Flashcards
Components of a gynae hx
Personal details
PC
Specific gynaecological questions
Past obstetric hx
Past medical hx
Systems r/v
DHx: allergies, penicillin and latex
FHx
Personal/Social hx
PC in G
SOCRATES
NOTEPAD
Impact on QoL
Previous consultations
Order multiple PCs in order of severity/impact on life
Menstrual questions in G Hx
FMP
How often, how many days from the first day of bleeding to the next first day?
How long does it last? (/28)
Is it regular or irregular
Heavy (number of pads, flooding, presence of clots)
Is it or the days leading up to it painful
IMB?
PCB?
Vaginal discharge- characterise
Does she experience premenstrual tension?
When was her LMP?
If post-menopausal, has there been PMB?
Sexual/contraceptive questiosn in G
Sexually active?
Painful- penetration (superficial dyspareunia) or deep inside (deep), during and or after (delayed)
What contraceptive does she use and has she used in the past?
Cervical smear questions in G
When was her last smear
Ever had an abnormal smear?
What was done?
Cervical screening
Every 3 years between 25 and 49
Every 5 years between 50 and 64
Not performed after 64 unless never screened or hx of recent abnormal tests
Urinary/prolapse questions in G
Frequency (normal is 4-7pd)
Nocturia
Urgency
Leak urine, including when asleep (nocturnal enuresis), if so how severe is it and with what is it associated (e.g. coughing, lifting/straining, urgency)
Dysuria?
Haematuria
Dragging sensation or feel a mass in or at the vagina?
Past obstetric hx in G
Have you ever been pregnant?
If yes ask about previous pregnancies in chronological order
Ask how infant was born, weight and how the infant is now. Name
Any major complications in pregnancy or labour?
PMHx in G
Previous gynaecological operations
Ask about DVT, DM, lung and CHD, HTN, jaundice etc as in other medical histories
Systems R/V in G
CV, Resp, Neuro.
Specifically ask about urinary and GI symptoms
FHx in G
FHx of breast, ovarian carcinoma?
DM?
VTE
CHD
HTN
Personal/social history in G
Smoke
ETOH
MarriedStable relationship
Support at home?
Where does she live and what sort of accomodation
Allergies in G
Ask specifically about penicllin and latex
Abdo exam in G
General examination: seek the systemic effects of gynaecological problems and assess general health.
Appearance and weight. T. BP. Pulse and possible anaemia, jaundice or lymphadenopathy.
Comfortably on back with head on pillow. Exposed from xiphisternum to pubic symphysis.
EMPTY BLADDER
Inspect: scars, body hair distribution, irregularities, striae and hernias
Palpate: tenderness, palpate the abdomen generally looking for masses. Then palpate specifically looking for masses from above the umbilicus down to the pubic symphysis. If masses are present, do they arise from the pelvis (can you get below them)
Percuss: look for shifting dullness
Auscultate: BS
Vaginal Examination
Rectal examination
Vaginal examination in G
Privacy, explain, use bathroom. Chaperone- name documented in the notes. Use lubricating jelly.
Inspect: vulva and vaginal orifices
Digital bimanual examination
Cusco’s speculum examination
Sim’s speculum examination
Digital bimanual exmaination
Assesses pelvic organs
Left hand on aboomen above the pubic symphysis and pushed down so the organs are palpated
Two fingers inserted into the vagina
Uterus: normally the size and shape of a small pear. Size, consistency, regularity, mobility, anteversion/retroversion and tenderness
Cervix: hard or irregular?
Adnexa: lateral to the uterus on either side. Tenderness and size and consistency of any amss assessed. Separate from the uterus
Pouch of Douglas: uterosacral ligaments should be palpable: even, irregular or tender, mass?
Cusco’s speculum
Allows inspection of the cervix and vaginal walls.
NB anteverted uterus.
Look for ulceration, spontaneous bleeding or irregularities.
Cervical smear
Slowly withdraw partly closing speculum to allow inspection of the vaginal walls to the introitus and rotate as retract
Sim’s speculum
Allows better inspection of the vaginal walls and te prolapse.
Patient in left lateral position.
Rectal examination
Appropriate if posterior wall prolapse, to distingusih between an enterocoele and a rectocoele and in assessing malignant cervical disease
May be necessary if a woman complains of cyclical rectal bleeding- ?rectovaginal endometriosis
What is thelarche and when does it begin?
Adrenarche?
Menarche
What controls secondary sexual characteristics?
Beginning of breast development: 9-11 y
Growth of pubic hair (11-12)
13y
Oestrogen
D1-4 mensturation
Endometrium is shed as hormonal support is withdrawn, myometrial contraction also occurs
D5-13 proliferative phase
GnRH stimulate LH and FSH which induce follicular growth
Follicle produces oestradiol and inhibin which suppress FSH.
As oestradiol level rise and reach their maximum they cause a +ve feedback on the hypothalamus/pit and cause LH surge.
Ovulation occurs 36 hours after the LH surge
Oestradiol also promotes endometrial proliferation
D14-28 Luteal/secretory phase
Follicle becomes corpus luteum, produces oestradiol but relatively more progesterone, which peaks d21-28
This induces secretory changes in hte endometrium.
Towards the end of the luteal phase, the corpus luteum starts to fail if the egg hasn’t been fertilised and oestradiol/progesterone levels fall.
This decline in hormonal support causes the endometrium to break down, leading to menstruation and the restart of the cycle
What can be used to delay menstruation and why?
Continuous administration of exogenous progesterone as it maintains the secretory endometrium
Normal mensturation cut offs
Menarche <16y
Menopause >45y
Mensturation <8d
Blood loss <80ml
Cycle length 23-25
No IMB
Menorrhagia
Heavy menstrual bleeding
IMB
Bleeding between periods
Irregular periods
Periods outside of the range of 23-35d with a variability of >7d between the shortest and longest cycle
Secondary amenorrhoea
Periods stop for 6m or more.
Oligomenorrhoea
Irregular periods, >35d-6m
PMB
Bleeding 1 year after the menopause
Dysmenorrhoea
Painful periods
Premenstrual syndrome
Psychological and physical symptoms worse during the luteal phase
Menorrhagia def
Excessive bleeding in otherwise normal menstrual cycle
Excessive menstrual blood loss that interferes with the woman’s physical, emotional, social and material QoL +/- other smyptoms
>80mL (corresponds to the maximum amount that a woman on a normal diet can lose without becoming Fe deficient)
Aetiology and epidemiology HMB (menorrhagia)
Rare causes of HMB
1/3rd women complain of HMB
Fibroids= 30% HMB
Polyps= 10% HMB
Thyroid disease, haemostatic disorders and anticoagulant therapy.
What differentiates bleeding in malignancy from HMB?
Bleeding in malignancy tends to be irregular
Hx in menorrhagia
Ex in menorrhagia
Menstrual calendar. Flooding and passage of large clots. Contraception.
Anemia. Pelvic signs often absent. Irregular enlargement of the uterus suggests fibroids.
Tenderness without enlargement suggests adenomyosis.
Ix in menorrhagia
FBC: to check patient’s Hb
TFTs/Coagulation: to exclude systemic causes (if there are factors indicating this may be the case)
Transvaginal USS of hte pelvis: to exclude local organic causes (endometiral thickness, exclude fibroid, mass and detect larger intrauterine polyps (+/- biopsy or hysterectomy if USS is inconclusive)
Indications for USS biopsy in HMB
Endometrial thickness >10mm
?Polyp
Woman >40 with recent onset menorrhagia
Treatment failure/ineffective treatment
Before insertion of IUS if cycle not regular
Prior to endometiral ablation/diathermy as tissue will not be available for pathology
If abnormal uterine bleeding has resulted in acute admission
Mx of HMB
Rx
Sx
Exclude pathology
Depends on woman’s contraceptive needs.
1st line= intrauterine system- not option for woman who wishes to conceive . 90% reduction in blood loss.
2nd line: antifibrinolytics (tranexamic acid) taken during menstruation only. 50% reduction in blood loss
NSAIDs (mefanamic acid) inhibit prostaglandin synthesis reducing blood loss by around 30%. NB also useful for dysmenorrhoea.
Combined OCP- lighter mesntruation but less effective if pelvic pathology is present.
3rd line: progestogens, high dose orally or by IM will cuase amenorrhoea but bleeding follows withdrawl.
GnRH agonists: produces amenorrhoea. Duration is limited to 6 months unless add-back HRT used.
Sx
Hysterposcopic:
Polyp removal (if caused by local abnormalities)
Endometrial ablation technique
Transcervical resection of fibroid (TCRF).
More radical:
Myomectomy
Hysterectomy:
Uterine artery ambolisation
Features of IUS
Progestogen impregnated IUD is a coil that reduces menstural flow with fewer Ses.
Highly effective alternative to medical and surgical treatment.
It is contraceptive and also provides the progestogen component of HRT.
Distinguish from Cu IUDs that may increase menstrual loss
Sx approaches to HMB
Hysteroscopic
More radical
Hysterposcopic:
Polyp removal (if caused by local abnormalities)
Endometrial ablation technique: removal/destruction of endometrium- satisfcation is less than with hysterectomy. Most appropriate in older women with pure menorrhagia. Non sterilising.
Transcervical resection of fibroid (TCRF).
More radical:
Myomectomy: removal of fibroids from the myometrium: open or laparoscopic (<4fibroids, <8cm diameter). Used if fibroids causing symptoms but fertility is still required. GnRH agonists can be used to reduce size of fibroids first.
Hysterectomy: last resort.
Uterine artery ambolisation: treats menorrhagia for women who want to retain their uterus.
Rx management of HMB
1st line: IUS
2nd line: antifibrinolytics, NSAIDs, OCP
3rd line: progestogens, GnRH analogues
When are anovulatory cycles common
Just after menarche and before the menopause
What are some causes of IMB/oligomenorrhoea
Anovulatory
Pathological:
Non malignant
Fibroids, uterine and cervical polyps, adenomyosis, ovarian cysts and chronic pelvic infection.
Malignant:
Overain, cervical and most particulalry endometrial
Ix in IMB/oligomenorrhoea
FBC: to asssess the effect of blood loss
Ix to exclude malignancy:
Cerbical smear
USS of the cavity for women >35 with irregular/IMB and in younger women if treatment has failed, will also detect uterine fibroid or ovarian mass.
Endometrial biopsy
Mx of Oligomenorrhoea/IMB
Rx
Rx where no anatomical cause is detected
1st line: IUS or OCP.
2nd line: 2nd line Rx for menorrhagia
Sx:
Cervicaly polyp can be excised.
Definition of Amenorrhoea
Absence of menstruation
1o= hasn’t started by 16, may be manifestation of delayed puberty in which secondary sexual characteristics are not present by age 14. If 2o sexual characteristics are present, problem of menstrual outflow is more likely.
2o= 6m without menstruation in previosly normal mensturation
Oligomenorrhoea: >35d-6m
Classification of causes of amenorrhoea
Physiological
Pathological
Physiological causes of amenorrheoa
Pregnancy, after the menopause, during lactation, constitutional dleay
Pathological amenorrhoea
Hypothalamus
Pituitary
Adrenals
Ovary
Uterus
Outflow Tract
Drugs
Hypothalamus: Hypothalamic hypogonadism.
Pituitary: hyperprolactinaemia; rarer= other pituitary tumours, Sheehan’s syndrome
Adrenal/Thyroid; hypo/hyperthyroid. CAH/virilising tumours
Ovary:
- Acquired: PCOS, premature menopause, rare virilizing tumours*
- Congnetial: Turner’s (most common), other forms of gonadal dysgenesis*
Outflow problems:
- Congenital: Primary amenorrhoea with normal secondary sexual characteristics. Imperforate hymen and transverse vaginal septum. Rokitansky’s syndrome*
- Acquired: Usually secodary. Cervical stenosis, Asherman’s syndrome, endometrial resection or ablation*
Drugs: e.g. antipsychotics, GnRH analgoues, progestogens
Hypothalamic hypogonadism
Mx
Common, usually due to psychologica, lowe weight or excessive exercise
Tumours are a rare cause and may be excluded by MRI.
GnRH and FSH/LH and oestradiol are reduced.
Bone density may be reduced if there has been prolonged hypo-oestrogenism.
Oestrogen replacement (+progesterone for endometrial protection) i.e. OCP/HRT
Hyperprolactinaemia
Mx
Usually caused by pituitary hyperplasia or adenomas
Rx: bromocriptine, carbegoline or Sx
Affect of hypothyroidism on prolactin levels
Hyperprolactinaemia leading to amenorrhoea
Turners Syndrome
45 XO
Short stature, poor secondary sexual characteritsics, normal intelligence.
Most common congenital ovarian cause of amenorrhoea
Haematoclpos
Haematometra
Accumulation of menstrual flow in the vagina
or uterus
To outflow tract obstruction by either imperforate hymen or transverser vaginal septum
Rokitansky’s syndrome
Mullerian agenesis
Congential malformation characterised by failures of Mullerian duct development resulting in a missing uterus and variable degrees of vaginal hypoplasia.
Mullerian agenesis is the aetiology in 15% of cases of primary amenorrhoea
Asherman’s syndrome
Consequence of excessive curettage in ERPC performed following miscarriage or delivery.
Asherman’s syndrome, also known as intrauterine adhesions, is a condition where the cavity of the uterus develops scar tissue (adhesions).
Mx of osteoporotic risk in primary amenorrhoea
Treat underlying cause
Asses # risk. Correct any VitDD and ensure adequate Ca intake.
Consider HRT.OCP if amenorrhoea persists for more than 12m
What blood results suggests premature ovarian failure?
Persistently elevated FSH and LH in woman younger than 40y/o
What factors are suggestive of Asherman’s syndrome
Recent Hx of uterine or cervical Sx or severe pelvic infection (endometritis)
Definition of PCB
Vaginal bleeding following intercourse that is not menstrual loss
Except for first intercourse, this is always abnormal and cervical carcinoma must be excluded.
Aetiology of PCB
When the cervix is not covered in health suqamous epithelium it is more likely to bleed after mild trauma.
What are the most common causes of PCB
Cervical ectropions
Benign polyps
Invasive cervical cancer
(cervicitis, vaginitis (atrophic)
Mx of PCB
Cervical inspection + smear.
Polyp- avulsed and sent to histology.
Ectropion can be frozen with cryotherapy.
Abnormal smear-> colposcopy
Def dysmenorrhoea
Painful menstruation. Associated with high PG levels in the endometrium and is due to contraction and uterine ischaemia.
Causes of dysmenorrhoea
Primary: when no orgnaic cause is found.
Secondary: when pain is due to pelvic pathology. Fibroids, adenomyosis, endometriosis, PID, ovariant tumours,
What differentiates between primary and secondary dysmenorrhoea?
Primary usually coincides with the start of mensturaiton and is very common, particularly in adolescents. Responds to NSAIDs and ovulation suppresions e.g. OCP. Pelvic pathology more likely if medical treatment fails.
Secondary: pain often precedes and is relieved by onset of menstruation. Deep dyspareunia and menorrhoagia or irregular mensturation are common. P USS and laparoscopy useful.
Def precocious puberty
When menstruation occurs before the age of 10 and/secondary sexual characteristics are evident before age of 8.
Causes of precocious puberty
Central
Ovarian/adrenal
In 80% no pathological cause is found.
Central causes: increased GnRH secretion: meningitis, encephalitis, CNS tumours, hydrocephaly and hypothyroieism may prevent normal prepuberatl inhibition of hypothalamic GnRH release. Rx:
Ovarian/adrenal causes: increased oestrogen secretion: hormone producing tumours of the ovary/adrenal glands. Regression occurs after removal. McCune-Allbright syndrome.
McCune-Albright syndrome
Bone and ovarian cysts
Cafe au lait sports
Precocious puberty
Mx of precocious puberty
GnRH agonists used to inhibit sex hormone secretion causing regression of secondary sexual health characteristics
For increased oestrogen secretion cypropterone acetate (antiandrogenic progestogen) can be used
CAH in genetic female
Aetiology
Features
Rx
Recessive inheritance.
Defective cortisol production usually as a result of 21-hydroxylase deficiency.
ACTH exess causes incresed androgen production.
Presents at birth with ambiguous genitalia. GC deficiency may cause Addisonian crisis.
May present at puberty with enlarged clitoris and amenorrhoea.
Cortisol and MC replacemant.
AIS in genetic male
Occurs when male has cell receptor insensitvity to androgen which are peripherally converted to oestrogens.
Individual appears to be female.
Presentation is with amenorrhoea.
Uterus absent, rudimentary testes present which are removed due to possible malginant change.
Premenstrual syndrome
Psychological, behavioural and physical symptoms that are experienced on a regular basis during te luteal phase of te mesntrual cycle and often resolve by the end of menstruation.
Hx in PMS
Cyclical nature rather than symptoms themselves that enable diagnosis.
Tnesion, irritability, aggressoin, depression, loss of control.
Bloatedness, GI upset, Breast pain
Ex in PMS
Menstrual diaries.
Psychological evaluation as depression and neurosis may present at PMS
Mx of PMS
SSRIs either continuously or intermittently in the second half of the cycle.
OCP.
GnRH agonists and add back oestrogens.
Supplements: evening primrose oil is good for breast tenderness. Pyridoxine 50mg BD can help but may cause neuropathy in excess
Vitex agnus-castus extract.
Anatomy of the uterus
Superiorly: fundus
Laterally to fundus= cornu which is the communication with the fallopiam tubes
Supported at the inferior end by the uterosacral and cardinal ligaments.
Anteverted in 80%
Wall is made of smooth muscle which is lined by endometrium (glandular epithelium)
Serosa= peritoneum posteriorly. Also covers the uterus down to the bladder. Laterally the peritoneum is continuouous with the broad ligaments that run between the uterus and pelvic side wall. These are continuous with the fallopian tubest and round ligaements suepriorly and inferiroly contain the uterine blood supply, ureturs and parametrium
Uterine blood supply
Lymph drainage?
From uterine arteries
Pass over the ureturs laterally to the cervix. Pass inferiroly and superiorly supplying the myometrium and endometrium.
Anastamose at the cornu with the ovarian blood supply.
Inferiorly anastamose with the blood supply to the upper vagina.
Lymph to EI Nodes.
Blood supply of the dnometrium
Spiral and basal arterioles.
Spiral= important in mensturation and nourishment of growing fetus.
After ovulation under the influence of progesterone during the luteal phase the glands swell and blood uspply increases.
Fibroids definition
Leiomyomata, bening tumours of the myometrium
25% of wmeon.
More common near menopause, Afrocaribbean and in FHx.
Less common in parous women and those who have taken OCP or injectable progestogens
Fibroid sites
Subsersal
Intramural
Submucosal may form intracavity polyps
Aetiology of fibroids
Oestrogen and progesterone dependant
Fbiroids regress after menopause
Hx in fibroids
50% asymptomatic and discovered at pelvic/abdo exams. Symptoms relate to site rather than size
Menstrual problems (30%): menorrhagia, unchanged timing of menses. IMB may occur if fibroid is submucosal or polypoid.
Erratic bleeding
Pain: dysmenorrhoea, seldom cause pain unless torsion, red degeneration or sarcomatous chnage occur
Pressure effects: large fibroids pressing on bladder can cause frequency/urinary retnetion.
Hydronephrosis due to ureteric compressoin.
Fertility impairment due to obstruction of the tubal ostia or submucous fibroids preventing implamantation. Intramural fibroids that aren’t distorting the cavity can also reduce fertility through an unknown mechanism.
Ex in Fibroids
Solid mass palpable on pelvic/abdo examination which arises from pelvis and is continuous with the uterus.
Multiple small fibroids cause irregular knobbly enlargement of the uterus.
Cx of fibroids
Enlargement: can be very slow. Often stop and calcify after menopause although HRT may stimulate further growth. Enlarge in pregnancy. Pedunculated fibroids may undergo torsion
Degenerations: result of inadequate blood supply.
Red degeneration (more common in pregnancy): pain + uterine tenderness, haemorrhage and necrosis
Hyaline/cystic degeneration the fibroid is soft and partly liquefied.
Malignancy: 0.1% are leiomyosarcomata. may be malignant change or de novo transformation of myometrium
Fibroids in pregnancy
Premature labour
Malpresentations
Transverse lie
Obstructed labour
PPH
Red degeneration
Pedunculated fibroids may tort in post partum period
Ix in Fibroids
Dx: USS bu MRI/Laparoscopy may be required to distinguish from ovarian mass
Adenomyosis can exist as a fibroid like mass (MRI ddx)
Hysteroscopy/hysterosalpingogram to assess distortion of the uterine cavity- if fertility is an issue.
To establish fitness: Hb may be low due to vaginal bleeding, may also be high
Why may Hb be high in fibroids
They can secrete EPO
Mx of fibroids
Asymptomatic with small/slow-growing: no treatment
Large fibroids that are not removed should be serially measured by examination or USS.
Menorrhagia associated fibroids:
<3cm without distortion of uterine cavity, determine whether woman wants to conceive and use treatment options for menorrhagia: LNG-IUS. Tranexamic, NSAID or OCPs
Norethisterone/Depoprovera (Progestetone)
>3cm: refer: Sx intervention. In interim can try NSAIDs/Tranexamic acid.
Compressive symptoms: refer
Fertility/obstetric symptoms: refer
Sx treatment of fibroid
Hysteroscopic: fibroid polyp or small submucous fibroid can be resected. Pretreatment with GnRH agonist for 1-2m can shrink the fibroid, reduce vasculairy and thin the endometirum making resection easier and safer
Myomectomy: open or laparoscopic. NB heavy blood loss and small fibroids may be missed. Myomectomy performed if medical treatment has failed but preservation of reproductive function is required. Preceded by 2-3m of GnRH agonist. Perioperative injection of vasopressin into the myometrium reduces blood loss.
Adhesions can form at site of myomectomy which can reduce fertility if affecting the endometrial cavity or fallopian tubes. if the endometrial cavity is opened during myomectomy, C-section is indicated in future pregnancy due to risk of rupture.
Radical hysterectomy: Pretreatment with GnRH, common indication. Laparoscopic, vaginal or open.
Other treatmnents:
UAE
Ablation
Def adenomyosis
Prsece of endometirum and its underlying stroma in the myometrium.
Found in 40% of hysterectomy specimens.
Associated with endometriosis and fibroids. Symptoms subside postmenopausally.
NB in anedomyosis
Endometrial tissues grows into the myometrium. Occassionally may show varying degrees of atypia or invasion
Hx of adenomyosis
Ex of adenomyosis
Symptoms may be absent but painful, regular, heavy menstruation is common.
Uterus is mildly enlarged and tender
Dx of adenomyosis
Not easily diagnosed on USS but can be diagnosed on MRI
Mx of adenomyosis
IUS
OCP +/- NSAIDs may control the menorrhagia or dysmenorrhoea but hysterectomy often required.
Oestrogen dependant.
Endometritis
Secondary to STI, as a complication of surgery (C-section and intrauterine procedure) or because of foreign tissue e.g. IUD and RPC.
Infection in the postmenopausal uterus is commonly due to malginancy
Hx and Ex in enodemtritis
Tender uterus with pelvic and systemic infection
Pyometra
Pus accumulates in uterus and is unable to escape
Mx of endometritis
Antibiotics
ERPC
Intrauterine polyps
Small bening tumours that grow in to the uterine cavity. Most are endometrial although some come from submucous fibroid.
Often found in patients on tamoxifen for breast Ca.
Occassionally contian endometrial hyperplasia or carcinoma.
Dx at USS/hysteroscopy
What is the most common genital tract cancer?
Endometrial carcinoma
Epidemiology or endometrial carcinoma
Highest prevalence >60
15% occur premenopausally.
<1% <35y/o
Usually presents early.
Adenocarcinoma of columnar gland cells >90%. Rest is adenosquamous carcinoma- poorer prognosis
What increases the risk of endometrial carcinoa?
high oestrogen: progesterone
When oestrogen therapy is used unopposed by progestogens
Risk factors for endometrial carcinoma
Protective
Exogenous:
oestrogens without a progestogen
Tamoxifen (acts as an agonist in the postmenopausal uterus)
Endogenous:
Obesity
PCOS as it is associated with prolonged amenorrhoea.
Nulliparity
Late menopause
Ovarian granulosa cell tumours (oestrogen secreting)
Misc: DM, HTN. Lynch Type 2 syndrome: familal non-polyposis colonic, ovarian and endometrial carcinoma.
OCP and pregnancy
Premalignant disease in endoemtrial carcinoma
Cystic hyperplasia-> Endometrial hyperplasia with atypia
May cause menstrual abnormalities or PMB
Often coexists (40%) with carcinoma elsewhere in the uterine cavity
Hx in endoemtrial carcinoma
Ex in endometrial carcinoma
PMB: 10% risk of carcinoma. Likelihood that PMB is due to cancer rather than unknown or benign causes increases with age. Premenopausal patients have irregular or IMB or occasionally recent-onset menorrhagia. Cervical semar may contain abnormal columnar cells.
Ex: pelvis often appears normal. Atrophic vaginitis may coexist
Spread of endometrial carcinoma
Through the moymetrium to the cervix and upper vagina. May be ovarian involvement.
Lymphatic spread to pelvci then para-aortic nodes.
Staging is surgical and histological and includes LN involvement
Endometrial carcinoma staging
Only possible post hysterectomy
1: lesions confined to uterus
A: <0.5 myometrial invasion.
B: >0.5 myometrial invasion
Stage 2: as above but in cervix too
Stage 3: Tumour invades through the uterus.
A: invades serosa or adnexae
B: vaginal/parametrial involvement
Ci: pelvic node involvement
Cii: para-aortic involvement
Stage 4: further spread
A: bowel or bladder
B: distant mets
Dx of endometrial carcinoma
USS/hysteroscopy- biopsy required to make diagnosis
MRI performe din all patients or if spread is suspected due to other symptoms.
CXR to exclude extrapulmonary sprad
FBC, RFT, glucose testing.
ECG
Treatment of endometrial carcinoma
Sx: 75% present with Stage 1. Hysterectomy and bilatreal salpingooophorectomy (BSO) is performed either open or laparoscopically.
Routine lymphadenectomy is not beneficial in early stage disase.
RTx: External beam radiography used following hysterectomy for those at high risk of LN involvement but not in those with early stage disease. RFs: deep myometrial spread, poor hisotlogy or grade, cerbical stromal involvement.
Vaginal vault therapy.
Other: Progestogens seldom used. CTx may have a role in high risk early stage and advanced disease.
Px for endometrial carcinoma
Poor pxic factors
Recurrency common at the vaginal vault.
Older age
Advanced stage
Deep myometrial invasion in Stage 1 and 2
High tumour grade
Adenosquamous hisotlogy
Uterine sarcomas
3 categories
Rare
Leiomyosarcomas: malignant fibroid
Endometrial stromal tumours: most common in perimenopausal woman
Mixed mullerian tumours: derived from the embryological elements of the uterus and more common in old age.
Usually present with irregular/PMB or rapid painful enlargement of a fiborid
Treatment with hysterectomy.
RTx/CTx can be used adjuvantly but 5 year survival is 30%
Px for Endometrial Ca by stage
1
2
3
4
1: 85
2: 70
3-4: 50
4:25
Overall 75
First line treatment for dysmenorrhoea?
NSAIDs as they will inhibit PG synthesis, one of the main cuauses of dysmenorrhoea pains.
First line treatment in urinary incontinence
Urge
Stress
Urge: bladder retrianing
Stress: pelvic floor muscle training
Causes of urinary incontinence
Overactive bladder/urge incontinence: due to detrusor overactivity
Stress incontinence: leaking small amounts when coughing or laughing
Mixed incontinence
Overflow incontinence: due to bladder outlet obstruction e.g. prostate englargement
Ix of urinary incontinence
Bladder diaries (>3d)
Vaginal examination to exclude cystocele
Urine dipstick and culture
Mx of urge incontinence
Conservative: bladder rtraining (lasts for minimum of 6w, idea is to gradually increase the intervals between voiding)
Rx: Bladder stabilising drugs: antimuscarinic is first line.
Sx: sacral nerve
Mx of stress incontinence
Pelvic floor muscle training (minimum of 3 months)
Srugical procedures e.g. retropubic mid-uretthral tape procedures
Common causes of vaginal d/c
Less common causes
Physiological
TV
BV
Gonorrhoea, Chlamydia (rarely PC), ectropion, foreign body, Cervical Ca
Features of Candida d/c
Cottage cheese
Vulvitis
Pruritis
Features of TV d/c
Offesnive, yellow/green, frothy d/c
Vulvovaginitis
Strawberry cervix
Features of BV d/c
Offesnive, thin, white/grey, fishy d/c
What differentiates between ectopic and threatened miscarriage
Ix
Mild suprapubic pain at 10w
USS
What is the typical symptom of urogenital prolapse
Bearing down, heaviness, dragging sensation
Cervical excitation is seen in?
PID and ectopic pregnancy
What is the classical history of ectopic pregnancy?
Amenorrhoea
Abdo pain
Vaginal bleeding
In combination with shoulder tip pain- peritoneal bleed
What are the types of miscarriage?
Threatened
Missed (delayed)
Inevitabel
incomplete
Features of threatened miscarriage
Painless vaginal bleeding before 24w (typically 6-9w)
Bleeding often less than mensturation
Cervical os is closed
Complicates 25% of pregnancies
Features of missed (delayed) miscarriage
A gestational sac which contains a dead fetus before 20w without symptoms of expulsion
Mother may have light vaginal bleeding/discharge and symptoms of pregnancy which disappear
Typically painless
Cervical os is closed
When the gestational sac is >25mm and no embryonic/foetal part can be seen it is sometimes described as a blighted ovum or anembryonic pregnancy
Features of inevitable miscarriage
Heavy bleeding with clots and pain
Cervical os open
Features of incomplete miscarriage
Not all products of conception have been expelled
Pain and vaginal bleeding
Cervical os open
Features of complete miscarriage
Spontaenous abortion with expulsion of the entire foetus through the cervice
Pain and uterine contractions stop after the foetus has been expelled
Dx: USS shows an empty uterus
In a female with PMB what is the diagnosis
A 72-year-old nulliparous female presents with post menopausal bleeding. She reports that her last cervical screening was 14 years ago. On examination she is found to be obese and hypertensive. What is the most important diagnosis to rule out?
Vaginal squamous cell carcinoma
Cervical squamous cell carcinoma
Endometrial adenocarcinoma
Atrophic vaginitis
Leiomyosarcoma
In a female with postmenopausal bleeding (PMB), the diagnosis is endometrial cancer until proven otherwise.
Although all the options can result in PMB, the question states the most important one to rule out, which in this case would be endometrial adenocarcinoma due to its strong association with PMB and the importance of an early diagnosis prognostically.
In addition, the patient in this question has two risk factors for endometrial adenocarcinoma - hypertension and obesity. Other risk factors include diabetes mellitus, polycystic ovarian syndrome, tamoxifen use, late menopause and high levels of oestrogen.
Ix of amenorrhoea
Exclud pregnancy
Gonadotrophins: low levels indicate hypothalamic cause whereas high levels suggest an ovarian problem (e.g. premature ovarian failure)
Prolactin
Androgen levels: raised may be seen in PCOS
Oestradiol
TFTs
What are the key signs and symptoms of endometriosis?
Cyclical abdo pain and deep dyspareunia, may be associated with fertility problems
What are the classifications of ovarian cysts?
Physiological: follicular, corpus luteum cyst
Benign germ cell tumours: dermoid cyst
Benign epithelial tumours: serous cystadenoma, mucinous cystadenoma
Featrues of follicular cysts
Commonest type of ovarian cyst
Due to non-rupture of the dominant follicle or failure of atresia in a non-dominant follicle
Commonly regress after several menstrual cycles
Features of corpus luteum cyst
If pregnancy doesn’t occur corpus luteum cyst usually breaks down and disappears, if this doesnt occur the corpus luteum may fill with blood or fluid and form a cyst.
More likely to present with intraperitoneal bleed than physiological cysts.
Features of dermoid cysts
Mature cystic teratomas: lined with epithelial tissue
Most comon benign ovarian tumour in woman under 30 years.
Bilateral in 10-20%
Usually asymptomatic
Torsion is more likely than with other ovarian tumours
Serous cystadenoma
Most common benign epithelial tumour which bears a resemblance to the most common type of ovarian cancer
Bilateral in around 20%
Mucinous cystadenoma
Second most common benign epithelial tumour
Large and amy become massive
If ruptures may cause pseudomyxoma peritonei
Pseudomyxoma peritonei
Pseudomyxoma peritonei (PMP) is a clinical condition caused by cancerous cells (mucinous adenocarcinoma) that produce abundant mucin or gelatinous ascites.[1] The tumors cause fibrosis of tissues and impede digestion or organ function, and if left untreated, the tumors and mucin they produce will fill the abdominal cavity. This will result in compression of organs and will destroy the function of colon, small intestine, stomach, or other organs. Prognosis with treatment in many cases optimistic,[2] but the disease is lethal if untreated, with death by cachexia, bowel obstruction, or other types of complications.
Disease most commonly caused by appendiceal primary cancer
A 22 year-old woman and her male partner present to their GP as they been unsuccessfully trying to conceive for 4 months. Her periods have been regular and there is no obvious cause in her history. What is the most appropriate next step in her management?
Refer the patient for a laparoscopy and dye test
Address how the couple are having sexual intercourse and reassure the patient
Refer the patient for a basal temperature test
Refer the patient for a luteal phase progesterone test
Refer the patient’s partner for semen analysis
A healthy couple can expect to take up to one year to conceive. Investigations are therefore usually performed after one year of regular attempts to conceive. It may however be prudent to address any mechanical reasons that are preventing the couple from conceiving, hence the sexual intercourse history.
Epidemiology of infertility
Infertility affects around 1 in 7 couples. Around 84% of couples who have regular sex will conceive within 1 year, and 92% within 2 years
What are the main causes of infertility?
Basic Ix
Male factor (30%)
Unexplained (20%)
Ovulation failure (20%)
Tubal damage (15%)
Other causes (15%)
Semen analysis
Serum progesterone 7d prior to expected next period
<16nmol/l serum progerstogen
Repeat, if consistently low refer to specialist
16-30nmol/l serum progestogen
Repeat
>30mnol/l serum progestogen
Indicates ovulation
Key counselling points to couples trying to conceive
Folic acid
BMI 20-25
Advise regular sexual intercourse very 2-3d
Smoking/drinking advice
Mx of abnormal cervical smears (around 5% of smears)
Moderate dyskaryosis
Severe dyskaryosis
Suspected invasive cancer
Inadequate
Moderate dyskaryosis: consistent with CINII, refer to colposcopy
Severe dyskaryosis: Consistent with CINIII refer to colposcopy
Suspected Invasive Ca: refer for urgent colposcopy
Inadequate: repeat smear, if 3 inadequate samples-> colposcopy
High risk HPV subtypes
16, 18 & 33
What are the causative organisms of PID?
Chlamydia- most common
N. Gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis
What are the features of PID?
Lower abdo pain
Fever
Deep dsypareunia
Dyuria and menstrual irregularities may occur
Vaginal or cervical discharge
Cervical excitation
Ix of PID
Screen for chlamydia and Dx
Mx of PID
Rx: oral ofloxacin + metronidazole
or
IM ceftriaxome and oral doxy and oral metronidazole
In mild cases of PID, IUD may be left in, however more recent guidelines suggest that removal of IUD may be assocaiteed with better ST outcomes
Cx of PID
Infertility
Chronic pelvic pain
ectopic pregnancy
Def of PID
Inflammation/infection of the female pelvic organs including the uterus, fallopian tubes, ovaries and the surroudning peritoneum. Usually as a result of ascending infection from the endocervix.
What is the action if a cervical smear shows borderline or low grade dyskaryosis?
If a cervical smear shows borderline or mild (low grade) dyskaryosis, the laboratory will also test the cytology sample for human papillomavirus (HPV). If HPV is found, the woman will be referred for colposcopy within 8 weeks. If HPV is not found, the woman will be returned to the routine screening programme
What are the USS features of adenomyosis
Imaging reveals a “boggy” uterus with subendometrial linear striations
What is Amsel’s criteria for the Dx of BV?
3/4 of:
thin, white homogenous d/c
clue cells on microscopy: stippled vaginal epithelial cells
Vaginal pH >4.5
Positive whiff test
A 53-year-old woman presents with urgency and frequency. Two weeks ago she consulted with a colleague as she felt ‘dry’ during intercourse. She has been treated for urinary tract infections on multiple occasions in the past but urine culture is always negative. Her only medication is continuous hormone replacement therapy. A vaginal examination is performed which shows no evidence of vaginal atrophy and no masses are felt. An ultrasound is requested:
Both kidneys, spleen and liver are normal size. Outline of the bladder normal. 5 cm complex ovarian cyst noted on left ovary. Right ovary and uterus normal
What is the most appropriate next step?
Refer for urodynamics
Pelvic floor muscle training
Trial topical oestrogen
Urgent referral to gynaecology
Refer for bladder retraining
Any ovarian mass in a post-menopausal woman needs to be investigated.- refer to gynae
Initial management for ovarian enlargement
What are the possible reports
USS
Unilocular- more likely to be physiological or benign
Complex- multilocular- more likely to be malignant
Mx of ovarian enlargement.
Depends on age and symptoms.
Premenopausal: conservative approach esp <35 as malignancy is less common. If the cyst is small (<5cm) and reported as simple- likely to be benign. Repeat USS in 8-12 w
Postmenopausal: physiological cysts are unlikely
any postmenopausal woman with an ovarian cyst regardless of nature or size should be referred to gynaecology for assessment
How can the risk of ovarian malignancy be calculated?
Serum Ca125
USS
Menopausal findigns
Definition of premature ovarian failure
Premature menopausal symptoms
Elevated gonadtrophin levels
<40y/o
Causes of premature ovarian failure
Idiopathic
Chemotherapy
Autoimmune
Radiation
Symptoms of premature ovarian failure
Climacteric symptoms: hot flushes, night sweats
Infertility
Secondary amenorrhoea
Raised FSH, LH
What is HRT?
Small dose of oestrogen combined with progestogen (in women with a uterus)
Side effects of HRT
Nausea
Breast tenderness
Fluid retention and weight gain
Potential Cx of HRT
Increaed risk of breast Ca (increased by addition of a progestogen)
Incresed risk of endometrial reduced by addition of a progestogen. Additional risk eliminated if a progestogen is given continuously.
Increased risk of VTE, increased by addition of a progestogen
Increased risk of stroke
Increased risk of IHD if taken more than 10 years after menopause
When does the risk of breast cancer in those taken HRT normalise?
After HRT has been stopped for 5 years
What are the features of chlamydia infection?
Asymptomatic in ~70% of women and 50% of men
Women: cervicitis (discharge, bleeding), dysuria
Men: urethral d/c, dysuria
Potential complications of chlamydia infection
Epididymitis
PID
Endometritis
Increased incidence of ectopic pregnancies
Infertility
Reactive arthritis
Perihepatitis (Fitz-Hugh Curtis Syndrome)
Dx of Chlamydia
NAAT
Urine: first void urine sample, vulvovaginal or cervical swab
Mx chalmydia
Doxycycline (7d) or azithromycin (1d)
If pregnant than erythromycin or amoxicillin
For women and asymptomatic men: all partners from 6 months should be contacted
For men: all partners from the 4 weeks prior to symptoms
Contacts should be treated presumptively
Anatomy of the cervix
2-3cm long made up predominantly of elastic connective tissue.
Attached posteriorly to the sacrum by the uterosacral ligaments and laterally to the pelvic wall by the cardinal ligaments.
Lateral to the cervix is the parametrium which contains conective tissue, uterine vessels and the ureturs
Lining of the endovervix
Lining of the ectocervix
What is the junction between these two types of cell?
Columnar (glandular) epithelium
Continuous with the vagina, covered in squamous epithelium
Squamocolumnar junction
What is the transformation zone
Clinical signficance?
Durign puberty and pregnancy, partial eversion of the cervix occurs.
The lower pH of the vagina causes the exposed area of clumnar epithelium to undergo metaplasia to squamous epithelium
Cells undergoing metaplasia are vulnerable to agents that induce neoplastic change and cervical carcinoma typically originates from this area.
Blood supply of the cervix
Lymph drainage
Upper vaginal branches of the uterine artery
Obturator and itnernal and external iliac nodes, then to common iliac and para-aortic nodes
What is the characteristic spread of cervical carcinoma?
Lymph and locally by direct invasion into the uterus, vagina, bladder and rectum
Features of cervical ectropion
In which people is it common?
Symptoms?
When the columnar epithelium of the endocervix is visible as a red area around the os on the surface of the cervix.
Due to eversion and is a normal finding in younger women
Those who are pregnant/taking the pill
Aysmtpomatic, may cause post-coital bleeding.
Mx of cervical ectropion
Cryotherapy following colposcopy to exclude carcinoma.
Exposed columnar epithelium is also prone to infection
Features of acute cervicitis
Rare
Results from STD
Ulceration and infection occasionally found in severe degrees of prolapse when the cervix protrudes
Features of chronic cervicitis
Chronic inflamamtion/infection, often of an ectropion
Causes vaginal discharge and may cause inflammatory smears
Cryotherapy +/- antibiotics dependant on culture
Features of cervical poylps
Age group
Smyptoms
Mx
Benign tumours of the endocervical epithelium
More common in women >40
May be asymptomatic or cause IMB/PCB
Small polyps are aveulsed and examined.
Still need to Ix bleedign abnormalities.
Features of Nabothian follicles
Occur where squamous epitelium has formed by metaplasia over endocevical cells.
The columnar cell secreaions are trappped and form retention cysts whcih appear as white/opaque swellings on the ectocervix.
Treatment not required unles symptomatic
Nabothian follicle
Cervical ectropion
What is CIN?
Cervical intraepithelial neoplasia
Presence of aytpical cells within the squamous epithlium
Dyskaryotic exchibiting larger nuclei with frequent mitosis
What is the grading of CIN?
CIN-I: mild dysplasia, atypical cells found in the lower third of the epithelium
CIN-II: moderate dysplasia, atypical cells foudn in the lower 2/3rds of the epithelium
CIN-III: Severe dysplasia, abnormal cells occupy the full thickness of the epithelium= Carcinoma in situ. Malginancy ensures if these abnromal cells invade through the BM
Px CINII/III
1/3rd will develop cervical cancer over the next 10 years.
Px of CIN-I
Least malignant potential, can progress but commonly regresses spontaneously.
When is the peak incidence of CINIII?
<45, 25-29 years old
Which strains of HPV are most frquently associated with cervical cancer? How many are considered high risk?
Types 16, 18, 31 and 33
13/130 different strains, are considered high risk
What strains are included in the UK HPV vaccination programme?
Types 16 and 18 as they are responsible for 75 of cervical cancer cases.
What other factors increase risk of CIN?
OCP
Smoking
Immunocompromised
Features of UK cervical screening programme
Every 3 years 25-49
Every 5 years 50-64
>65: offer if they have not had a cervical screenign test since 50 years old or a recent cervical cytology sample is abnormal
What is CGIN?
What must then be excluded
Cervical glandular intraepithelial neoplasia
Adenocarcinoma of the cervix of endometrium should be excluded using both colposcopy and endocervcal curettage or with cone biopsy. Hysteroscopy can be used.
Mx of abnromal smear
Normal: continue with normal screening
Borderline/mild dyskaryosis: HPV triage: if negative, back to routine recall. If +ve-> colposcopy
Moderate dyskaryosis: colposcopy
Severe dyskaryosis: urgen colposcopy
CGIN: colposcopy, if abnormality not found-> hysteroscopy
Mx of CINII/III
LLETZ (large loop excision of transformation zone) aka diatheyrmy loop excision.
What are the major common complications of LLETZ?
Postoperative haemorrhage- uncommon
Risk of subsequent preterm delivery is increased
Discussion of abnormal smear with patient
Assume they have cancer- reassure about early warning cells.
CINIII- without treatment she has a 30% chance of developing cancer over 8-15 years.
Which type of cervical malignancy has a worse prognosis?
Adenocarcinoma
What is occult cervical carcinoma?
When there are no symtposm but the diagnosis is made by biopsy or LLETZ
Hx in clinical cervical carcinoma?
Ex?
PCB, IMB, PMB, an offensive vaginal discharge. Pain is not an early features but later disease which involves ureturs, bladder, rectum and nerves can cause: uraemia, haematuria, rectal bleeding an pain. Smears have usually been missed.
Ulcer or mass may be vissible or palpable on the cervix
Spread of cervical cancer
Locally: parametrium and vagina and then to the pelvic side wall. Lymphatic spread to the pelvic nodes is an early feature. Ovarian spread is rare with squamous. Haematological spread is later.
Staging of cervical carcinoma
NB limited due to lack of inclusion of LNs as prognostic consideration
Stage 1: confined to cervix
Stage 2: Invasion into the vagina but not the pelvic side wall
Stage 3: invasion of the lower vagina or pelvic wall or causing ureteric obstruction
Stage 4: invasion of blddder or rectal mucosa or beyond the true pelvis
Ix in cervical carcinoma
Dx: Tumour biopsy
Vaginal and rectal ecam to assess teh size of the lesion and local invasion. Examination under anaesthetic is performed
Cystoscopy for bladder involvement.
MRI detects size, spread and LN involvement.
To assess patient’s fitness for sx: CXR, FBC and U&Es.
Treatment of Stage 1aicervical malignancies
Stage 1ai with cone biopsy.: postoperative haemorrhage and preterm labour are the main complications. Simple hysterectomy preferred in older women.
Treatment of Stage 1 and 2 cervical malignancy that isn’t stage 1ai
Sx or CTx
CTx or RTx if: +ve LNs on MRI or after lymphadenectomy.
If LNs -ve as an alternative to hysterectomy
Surgical resection margins not clear
Palliation for bone bain/haemmorrhage.
Sx: Wertheim’s hysterectomy if LNs not involved. Ovarias left in young monan with squamous carcinoma. Cx: haemorrhage, ureteric and bladder damage, lymphocyst
Radical trachedectomy is less invasive procedure for women who wish to conserve fertility. (LNs negatvie|)
Wertheim’s hysterectomy
Radical abdominal hysterectomy
Involves node clearance, hysterectomy and removal of parametrium and upper 1/3rd of vagina
Younger women with squamous carcinom are left with ovaries
Radical trachedectomy
Removal of 80% of cervix and upper vagina
To preserve fertility
Stage 2b and worse or +ve LNs
RTx and CTx with platinum agents
Mx Recurrent cervix tumours
CTx/RTx
Pelvic exenteration can be considered if the disease is central.
Pelvic exenteration
Removal of the vagina, the uterus and cervix, the bladder and or the rectum
Px for cervical Ca
1a
1b
2
3-4
LNs involved
LN-ve
Overall
95
80
60
10-30
+ve 40
-ve 80
Overall 65
Poor pxic indicators in cervical malignancy
LN +ve
Advanced stage
Large priamry
Poorly differentiated tumour
Early recurrence
What is usually the cause of death in cervical carcinoma?
uraemia due to ureteric obstruction
Stage 1ai/1aii/b in cervical cancer
ai <3mm depth, <7mm across
aii <5mm depth, <7mm across
bi clnically visible lesion, greater than ai <4cm in greatest dimension
bii clinically visible lesin, <4cm
Stage 2ai/aii/b in cervical cancer
ai Involvement of upper 2/3rds of vagina without parametrial invasion <4cm
aii <4cm
b Invasion of parametrium
Componenets of an obstetric history
Pesronal details
PC/HPC
Hx of present pregnancy
Past obstetric Hx
Other Hx: past gynaecological hx, PMH, ROS, DHx, FHx, Social Hx, Allergies, VTE risk
PC in ObHx
Why is she in hospital?
Common reasons: HTN, pain, antepartum haemorrhage, unstable lie, possible ROM.
If the pregnancy has hitherto been uncomplicated, mention this
Hx of present pregnancy
Dates: What was the first day of her LMP
What was the length of her menstrual cycle, regular?
How many weeks gestation (38w= 36w since conception)
EDD: Nagle’s rule
Complications of pregnancy: bleeding, HTN, DM, anaemia, urinary infections, conern about fetal growth, other problems. Ask about hospital admissions during the pregnancy
Tests: what tests have been performed e.g. USS, blood tests, prenatal Dx tests
Nagle’s rule
Subtrate 3m from the date of the LMP, add 7d anjd one year.
NB if a cycle <28d, the EDD will be later and needs to be adjusted (add the number of days >28 to the date calculated using Nagle’s rule.
Same applies if shorter.
When is the USS dating performed?
11-13w+6
USS measurments to date pregnancy
Measurement of crown-rump length between w9 + 14
Head circumference between 14-20w if no early scan and LMP unknown.
NB of little use after 20w.
What is a consideration re EDD and women recently stopping OCP
Her cycles can be anovulatory and LMP is less useful
Past ObHx
Details of past pregnancies in chronological order.
Mode and gestation of delivery, if operative, why?
Birth weight and sex of the baby
Mother/baby had any Cxs?
Parity
Gravidity
Parity
Number of times a woman has delivered potentially viable babies (>24w)
Suffix denotes number of pregnaniecs that have miscarried or been terminated prior to 24w.
Nulliparous
Never delivered a potentially live baby, she may have had miscarriages or abortions
Muktiparous
Delivered at least one baby at 24w or more
Gravidity
Describes the number of times a woman has been pregnant.
PGHx in OBHx
Last cervical smear
Treated for an abnormal smear
Prior contraception
Difficulty conceiving
PMHx in ObJx
Surgeries
CHD
HTN
DM
Psychiatric disease
Epilepsy
FHx in OBHx
FHx of twins?
DM
HTN
Pre-eclampsia
Auto-immune disease
VTE or thrombophilia
Any inherited disorders
SHx in ObHx
Smoke
Drink
Drugs
Stable relationship? Social support
Domestic abuse
Palpation of the abdomen and what it tells you at
<24w
>24w
>36w
Dates, twins
Well-being by assessing size and liquor
To check lie, presentation and engagement
Ob Ex
General examination
Abodminal Examination
Consider examination of fundi, reflexes, T, epigastrium, legs, chest etc.
General examination in obstetrics
Appearance, T, oedema, anaemia
Height and weight
Chest, breasts, CVS examined
BP and urinalysis
Diastolic BP is recorded at as Korotkoff V: when the sound disappears
Abdominal examination in pregnancy
When is the uterus palpable?
Where is it found?
Semi-prone. Exposed from below the breasts to the symphysis pubis. Later pregnancy can include left lateral tilt to avoid aortocaval compression
Uterus normally palpable at 12-14w.
20w: umbilicus
What may be the cause if a uterus is larger than expected before 20w?
Incorrect dates, full bladder, multiple pregnancy, uterine fibroids, pelvic mass
Ob Ex
I
P
P
A
I: size of pregnant uterus, look for striae, linea nigra and scars in the suprapubic area. Fetal movements often visible in later pregnancy
Palpation: us the fetus adequately grown, is liquor volume normal? what is the lie? What is the presentation?
Ausculation: listening over the anterior shoulder the fetal heart should be heard with a Pinard’s stethoscope, should be 110-160bpm
Steps in palpation
- Find the funduse using the fingers and the ulnar border of the left hand. Measure the distance to the pubic symphysis with a tape measure. (after 24w this corresponds to the gestation +/- 2cm. Best for small for dates but only 70% sensitive. Look for tenderness or uterine irritability
- Use both hands to palpate down the fetus towards the pelvis using dipping movements to palpate the fetal parts and liquor volume. Polyhydramnios: bag will be tense and will need to dip far to feel anything. Head can be balloted, breech is softer and cannot be balloted. Lie: longitudinal, transverse, oblique (head/buttocks palpable in one of the iliac fossae)
- Turn to face the pelvis and press both hands firmly down to assess the presentation. Engagement of the head occurs when the widest diameter descends into the pelvis and is describe as fifths palpable.
Fifths palpable
2/5ths= engaged
Pawlik’s grip
Grasp the presenting fetal part between the thumb and index finger of the examining hand. Uncomfortable and seldom necessary
Findings in Ob Ex
Uterine Size: fundus palpable at 12-14w. Umbilicus at 20w. Xiphoid sternum at 36w. Fundal height increases 1cm/week after 24w
Presentation: Breech in 20% at 28w. 3% after 37
Engagement: usual in nulliparoius after 37w. Multiparous often not engaged
Presnting Ob Ex
Gynae Ex presentaiton
Definition of preterm delivery?
Whenare risks greatest?
24-37w
<34w
What are the complications of preterm delivery for the neonate?
Prematurity accounts for 80% of NICU occupancy
20% of perinatal mortality
up to 50% of cerebal palsy
Chronic lung disease
Blindness
Minor disability
What are the risks at 24w to neonate of preterm delivery?
1/3rd handicapped
1/3rd will die
What are the complications of preterm delivery to the mother?
Infection
Endometritis
C-section
Risk factors for spontaneous preterm labour
Complications of pregnancy
Maternal medical disease
Maternal demographs
Previous Hx
Lower socioeconomic class
Extremes of materanl age
Short inter-pregnancy interval
Maternal medical disease: renal failure, diabetes, thyroid disease
Pregnancy complications: pre-eclampsia, IUGR, male fetal gender, raised Hb, STIs and vaginal infection (BV), previous cerbical surgery, multiple pregnancy, uterine abnormalities, fibroids, UTIs, polyhydramnios, congenital fetal abnormalities, APH
Mechanisms of spontaneous preterm labour
Multiple pregnancy
Delivery before 34w occurs in 20% of twins and is the mean delivery of triplets
Excess liquor, polyhydramnious has the same effect, probably largely mediated by increased stretch
Mechanisms of preterm labour
Fetal survival response
More common when fetus is at risk: pre-eclampsia and IUGR or there is infection
Placental abruption often followed by labour
Iatrogenic preterm delivery aims to improve upon this mechanism
Mechanisms of preterm labour relating to the reproductive system
Uterine abnormalities e.g. fibroids or congenital abnormalities
Cervical incompetence: some follows previous surgery for CIN or multiple dilatations of the cervix, but in others cause is unknown
What are the manifestations of infection in pregnancy?
Chorioamnionitis, offensive liquor, neonatal sepsis and endometritis
What infective pathogens are risk factors for preterm delivery?
What is often seen in preterm delivery caused by infection?
BV, GBS, Trichomonas, Chlamdyia, (commensals)
Coexisting cervical component
Hx for predicting preterm labour
Those at increased risk
Particulalry those with previous Hx of late miscarriage or preterm labour
Most women are not identified as high risk on Hx alone
Ix for predicting preterm labour
Cervical length on transvaginal sonography is sensitive and specific
Defined as from the external to the internal os
Prevention of preterm labour
Cervical cerclage (vaginal or abdominal route) usually preprgancny. Ca be used as prophylaxis, prevention or as a “rescue suture” when an incompetent cervix is dilated
or
Transvaginal progesterone suppositaries
or
?antibiotics
or
fetal reduction
or
treatment of polyhydramnios through needle aspiration or NSAIDs (if fetal surveillance is intensive) as they reduce fetal urine output
or
treatment of medical disease
NICE guidlines prophylaxis of preterm
Vaginal progesterone or prophylactic cerclage to women:
with Hx of spontaneous preterm birth or midtrimester loss between 16 and 34w and in whome a TVUS has been carried out between 16 and 24w of pregnancy and has revealed a cervical length <25mm
Prophylactic vaginal progesterone to women with no Hx of spontaenous preterm bith or miscarriage in whom a TVUS has been performed and reveals a cervical length of <25mm
Consider cerclage in women who have had a TVUS which reveals a cervical length <25mm and who have had P-PROM or Hx of cervical trauma
When is shortened cervical length picked up on TVUS?
What is the measurement?
16-24w
25mm
What is a consideration for NSAIDs in the foetus?
Can cause premature closure of the FDA
What are the contraindications for rescue cervical cerclage?
Indications?
Signs of infection or active vaginal bleeding or uterine contractions
16-27+6w with a dilated cervix and exposed unruptured fetal membranes.
Hx in preterm labour
Painful contractions, these will stop spontaneously in half of women
With cervical incompetence, painless cervical dilatation may occur and woman may experience a dull suprapubic ache or increased discharge
Antepartum haemorrhage and fluid loss are common, the latter suggesting ROM
Examination in preterm labour
Fever
Lie and presentation may be checked
Digital vaginal examination is performed unless the membranes have rupture
An effaced or dilating cervix confirm the Dx but the course of preterm labour is unpredictable
Ix in preterm labour
Cardiotocography and USS to assess fetal state
To assess likelihood of delivery: if cervix is effaced fetal fibronectin is helpful. TVS of cerbical length is alos predictive, >15mm means unlikely
Look for infection: vaginal swabs, CRP, WCC (NB steroids will cause it to rise)
Broad Mx of preterm labour
Steroids given 24-34w, in those presenting with contraction these can be restricted to women who are fibronectin +ve or have a short cervix, these reduce perinatal morbidity and mortality by promoting pulmonary maturity. NB glucose control. As they take 24h to take effect delivery is often delayed using tocolysis. Repeated doses not recommended
Tocolysis: nifedipine or atosiban (oxytocin-R antag) can be given to allow steroids time to act or to allow transfer to a unit with NICU. Delay rather than stop labour and shouldn’t be used for more than 24h.
Detect and prevent infection
Mg Sulphate: neuroprotective for the neonate if given prior to delivery. NB toxic in OD.
Mode of delivery in preterm labour
Mode of delivery in preterm labour
Vaginal delviery reduces NRDS. Caesarian undertaken only for obstetric indications. Breech is more common in preterm laour
Conduct of delivery: membranes are notruptured in membrane. Labour may be slow allowing steroids more time to act. Forceps rather than ventouse are used. Unless immedaite resuscitation is required the cord should not be clamped for 45s.
Antibiotics are recommended in actual as opposed to threatened preterm labour due to increased risk and morbidity of GBS
NICE Dx of preterm
<30w clinically suspected preterm labour: treat
>30w: TVU measurment of cervix, >15mm unlikely preterm labour. Think of alternative dxs. <15mm treat for preterm
If TVS not available, fetal fibronectin +ve: treat, -ve: unlikely in preterm.
Do not use TVS and fetal fibronectin in combination to Dx preterm labour
NICE Mx of preterm labour
Nifedipine or oxytocin antagonist (atosiban)
Maternal corticosteroids
Mg Sulphate
Definition of preterm prelabour ROM (P-PROM)
Membranes rupture beofre labour at <37w
All the causes of preterm labour may be indicated
It occurse before 1/3rd of preterm deliveries
What are the Cxs of P-PROM?
Preterm deelivery and follows within 48h of >50% of cases
Infection of fetus or placenta (chorioamnionitis) or cord (funisitis) is common. May be the cause and thus occur before or it may follow
Prolapse of the umbilical cord may occur rarely
Absence of liquor <24w can result in pulmonary hypoplasia and postural deformities
Hx and Ex in P-PROM
Gush of clear fluid followed by further leaking
Ex: lie and presentation are checked.
Dx is with a pool of fluid in the posterior fornix on speculum examination
Digital examination to exclude cord prolapse if the presentation is not cephalic
What are the clinical features of chorioamnionitis?
Contractions or abdo pain
Fever
Tachycardia
Uterine tenderness
Coloured or offesnive liquor
Ix in P-PROM
Speculum examination, if pooling not observed consider IGF binding proetin 1 test or placental microglobulin-1 test of vaginal fluid
If the results are positive, in conjunction with clinical presentation, offer management in keeping with woman having P-PROM,
If negative, unlikely she has P-PROM
Mx of P-ROM (NICE)
Balance risk of infection with risk of preterm delivery.
Identify infection: CRP, WCC, CTG, do not use in isolation
Prophylactic antibiotics: Erythromycin (250mg QDS for <10d or until labour). If erythromycin is CIed consider oral penicllin.
Close maternal and fetal surveillance, if gestation reaches 36w, induce labour
Why is co-amoxiclav contraindicated in P-PROM as an antibiotic prophylaxis?
Increases risk of NEC in neonate.
What are the normal blood changes in pregnancy an and why?
Normally falls to a minmum in the second trimester by about 30/15
Occurs in both normal and chronically hypertensive women due to a reduction in SVR
Rises again by term to normal pre-pregnant levels
What is the normal increase in protein excretion in pregnancy?
<0.3g/24h
What is the definition of PIH?
When the blood pressure rises by 140/90
Can be either pre-eclampsia or transient HTN
Normally after 20 weeks
What is pre-eclampsia
HTN and proteinuria (>0.3g/24h)
Appears in hte second half of pregnacny normally with oedema
Occasionally proteinuria is absent in early stage of disease
What is pre-existing HTN
What are the implications?
BP >140/90 before pregnancy or before 20w gestation or if the woman is on antiHTNs
May be 1o or 2o to other disease
May also be pre-exisitng proteinuria because of renal disease
What are the implications of pre-existing HTN on pre-eclampsia?
6x risk of “superimposed” preeclampsia
What is the course of pre-eclampsia
HTN normally precedes proteinuria which is a relatively late sign
Variability in time and severity of presentation.
The degree of HTN can be used to help asses it
Early onset disease tends to be more severe, after delivery may take up to 24h for “cure”
Pre-eclampsia epidemiology
6% of nulliparous. Less common in multiparous unless additional risk factors are present
What is the recurrence rate of pre-ecl
15% but can be up to 50% if there has been severe disease before 28w.
What are the 2 stages of pre-eclampsia pathogenesis
Stage 1: occurs before 20w. Incomplete invasion of spiral arterioles by trophoblasts leading to decreased uteroplacental blood flow.
Stage 2: manifestation of disease. Ischaemic placenta induces widespread endothelial cell damage causing vasoconstriction, increased permeability and clotting dysfunction.
What are the principal risk factors for pre-ecl
Nulliparity
Previous Hx
FHx
Old maternal age
Disorders characterised by microvascular disease: chronic HTN, chronic renal disease, SCD.
DM
Pregnancies with large placenta: Twin pregnancies, molar, fetal hydrops
Autoimmune disease (esp antiphospholipid)
Renal disease
Obesity
What are the classifications for HTN in pre-ecl
And pre-eclampsia itself?
>140/90= mild
>150/100= modetae
>160/100= severe
Mild: proteinruia and mild/modearate HTN
Moderate: proteinuria and severe HTN with no maternal complications
Severe: proteinuria and HTN <34w or with maternal complications
What are the protein cut offs in pre-ecl?
Dipstick
PCR
24h
Trace: seldom significant
+1: possible significant, quantify
+2: likely significant, quantify
PCR >30mg/noml: confirmed significant proteinuria
24h collection: >0.3g.24h
Hx of pre-eclampsia
Ex
Usually asymptomatic, headache, drowsiness, visual disturbances, N+V or epigastric pain may occur at late stage
HTN usually first sign but occasionally absent
Oedema may be massive, not postural or of sudden onset
Epigastric tenderness suggestive of impending complications
Urine dipstick
What are the maternal complications of pre-eclampsia?
Eclampsia: grand mal seizures. Mortality can result from hypoxia and concomitant complications. Rx with Mg SO4
CBA: results from failure of cerebral blood flow autoregulation, antiHTNsives can help
Liver and coag problems: HELLP syndrome. DIC, liver failure and rupture may occur. Treatment is supportive and may incude MgSO4 prophylaxis
Renal failure: fluid balance monitoring, may require haemodialysis
Pulmonary oedmea: Severe pre-eclamptic is particulalry vulnerable to fluid overload. PO treated with O2 and frusemide, assisted ventilation. ARDS may develop.
What are the fetal complications of pre-ecl?
Perinatal mortality and morbidity are all increased. Stil birth
<34w: IUGR, spontaneous preterm labour. Preterm devliery often required
Term: affects grwoth less but still associated with increased morbidity and mortality
At all gestations there is an increased risk of placental abruption
Dx of pre-ecl
Monitoring of pre-eclampsia
If dipstick positive exclude UTI with cultures and quantiy proteins.
Blood tests: Hb often high, uric acid elevated. Rapid fall in platelets suggests impending HELLP.
ALTs suggest impending liver test or help. LDH levels rise with liver disease and haemolysis
RFT: rapidly rising creatinine suggests severe Cxs and renal failure
Fetal: USS, umbilical artery doppler and if abnromal CTG to evaluate fetal well-being
HELLP syndrome
Haemolysis
Elevated Liver enzymes
Low Platelets
Screening for pre-ecl
HTN and urinaylsis checks in all pregnant women, esp those at high risk.
Most common is uterine artery Doppler at 23w.
Preventing pre-eclampsia
High risk women: 75mg of aspirin OD from 12w until birth of baby
What factors indicate women should be on aspirin for pre-eclampsia risk?
HTN disease during previous pregnancy, CKD, Autoimmune disease, DM, chronic HTN= High risk
first pregnancy, >40y/o, pregnancy interval of more than 10 years, >BMI, FHx, multiple pregnancy= moderate risk, >1 of these=aspirin
What are the indications for hospital admission according to NICE in pre-ecl
Mild, moderate or sever HTN= admission
Significant proteinuria
Following admission, should have regular BP monitoring, repeat quanitifcation of proteinuria not necessary. Montor RFT, FBC, LEs
What is first line treatment for pre-ecl HTN?
Which severities?
Labetalol
Moderate and severe, to keep DBP between 80-100 and systolic to <150
Mx of severe HTN or pre-eclampsia
Anticonvulsants: IV Mg SO. Loading dose of 4g followed by a 24hr infusion
Anti-HTNs: labetalol (oral or IV), hydralazine (+/- hydralazine) (IV), nifedipine
Corticosteroids for fetalo lung maturation: betamethasone (if <34w)
What are the adverse effects of MgSO4
Severe respiratory depression and hypotension
Preceded by loss of patellar reflexes
NB renal impairment, stop
Timing of delivery for pre-eclampsia
<34w: after discussion with neonatal and anaesthetists and course of corticosteroids if sever HTN develops refractory to Rx. Maternal or fetal indications.
>34w when BP has been controlled and if corticosteroid course complete
34-36+6: depnding on fetal condition
>37w: within 24-48h of onset
Conduct of delivery in pre-ecl
<34w: Csec
>34w: labour can be induced with PGs, epidural analgesisa helps reduce BP.
Use anti-HTNs
determine need for haematological and biopchemical tests.
Do not rountiely limit second stage of labour.
if HTN is severe and refractory to treatment, recommend operative birth
Post-natal care in pre-ecl
BP: monitor, ask about symptoms each time BP is measured.
Monitor bloods
Monitor fluid balance. NB PO and ARDS. If urine output is persistently low, use CVP monitoring. If CVP is high (overload) frusemide. If low, fluid but not albumin. If normal and oliguria persists renal failure is likely, K levels indicate need for dialysis
BP maintained at 140/90, postnatal treatment is with beta-blocker, nifedipine and ACEI can be seocodn line
Aetiology of pre-pregancy 2o HTN
Obesity, DM, renal disease (PCD, RAS, chronic pyelo)
Rarer include phaeo, Cushing’s, cadiac, coarctation
What should be exluded in all hypertensives?
Fundal changes, renal bruit, radiofermoal delay.
Ix in pre-existing chronic HTN in pregnacny
To identify secondary HTN, exlude Pheoe as maternal mortality is very high (24h VMA)
Look for coexistant disease through renal USS and RFTs
Identify pre pregnancy degree of proteinuria to alloiw compairosn later in the pregnancy
Mx of pre-pregnancy HTN
Stop ACEI and ARBs due to teratogenicity. Labetalol. Nifedipine second line.
Keep dietary Na low.
Kepp BP <150/100.
If HTN is severe and refractory offer birth.
Screen for pre-ecl
Low dose aspirin.
Mx of PIH
Take account of additional RFs
If HTN is sever admit until moderate levels.
Monitor proteinruia at each visit.
Labetalol, second line nifedipine, methyldopa
Do not offer birth to <36w unless HTN is severe.
Def: APH
Bleeding from genital tract after 24w gestation.
What are the causes of APH?
Common:
Rarer:
Undetermined origin, placental abruption, placenta praevia
Incidental genital tract pathology, uterine rupture, vasa preavia, placenta praevia
Def: placent praevia
Epidimeology
How does it change?
Occurs when the placenta is implanted in the lower segment of the uterus
Complicates 0.4% of pregnancies at term.
At 20w the placenta is low-lying in many more pregancies but appears to move upwards as the pergnancy continues, only 1 in 10 apparently low-lying placenta will be praevia at term.
How can placenta praevia be classified?
Marginal (I-II): placenta in lower segment, not over os
Major: placenta completely or partially covering os
What increases the risk of placenta praecia?
Twins, age of mothers, uterine scarring
What are the cxs in placenta praevia?
Obstructs engagement of the head, may necessitate C-sec and cause transverse lie
Haemorrhage can be severe and may continue during and after delivery as the lower segement is less able to contract and constrict the maternal blood supply.
If placenta implants in previous c-sec scar it may be so deep as to prevent placental separation or even penetrate through the uterine wall into the surrounding structures such as the bladder (placenta accreta and placenta percreta respectively). May provoke massive haemorrhage at delivery and require hysterectomy.
Hx and Ex in placenta praevia
Intermittenet painless bleeds which increase in frequency and intensity over several weeks. (1/3rd won’t have experienced bleeding before delivery)
Ex: breech presentation and transverse lie. No fetal head engagement. Vaginal examination can provoke massive bleeding and is never performed in a woman who is bleeding vaginally until placenta praevia has been excluded.
May be found incidentally on USS
Ix of placenta praevia
USS
Most diagnosed prior to bleeding, if low lying placenta has been dxed at a 2nd trimester USS this is repeated vaginally at 32w to exclude praevia. A placenta <2cm from the itnernal os is likely to be praevia at term. If close to a previous c-sec scar, 3-d power USS is best to determine if there is placenta accreta.
CTG
FBC: clotting studies and cross-match
Mx of placenta praevia
Admit all women with bleeding. If placenta praevia is found on USS women often stay in hospital until delviery due to risk of haemorrhage.
Blood kept available.
IV access maintained
Steroids if <34w.
If asymptomatic can delay until 37w.
Delivery: C-sec at 39w by most senior person available. Intra-operative and PPH are common.
May be emergency if bleeding is severe.
Accreta or percreta should have been anticipated although it may occur without invasion through a scar. Uterine incision should be made away from the placenta which can be left in situ or hysterectomy. Treatment of haemorrhage can be with compression of the scar after placental removal through a Rusch balloon. Alternatively, hysterectomy
Def: placental abruption
When part or all of the placenta separates before fetal delivery. Occurs in 1% of pregnancies
Pathology of fetal abruption
Placenta separating may lead to considerable maternal bleeding. Can lead to further placental separation and acute fetal distress.
Blood revealed as APH
May also enter the liquor
Or the moyemtrium (visible haemorrhage is absent in 20%)
Types of palcental abruption
Revealed
Concealed: bleed into the myometrium
Cxs of placental abruption
Fetal death (30% of proven abruptions)
Haemorrhage often necessitates blood transfusion: DIC and renal failure may lead to maternal death
What are the risk factors for abruption?
IUGR
Pre-ecl
Pre-existing HTN
Maternal smoking
Hx of placental abruption (6% risk)
Autoimmune diesase
Cocaine usage
Multiple pregnancy
High maternal parity
Trauma
Sudden reduction in uterine volume (ROM in woman with polyhydramnios)
Hx and Ex in placental abruption
Painful bleeding, often dark. Degree of vaginal bleeding does not reflect severity of the abruption. If pain occurs alone= concealed
Ex: tachycardia suggests profound blood loss. hypotension after massvie loss, uterine tender and often contracting. In severe cases the uterus is woody hard and the fetus difficult to palpate. Fetal heart tones abnormal/absent. If coagulation failure has occured, widespread bleeding is evident
Ix of placental abruption
Clinical dx
Ixs help to establish severity and plan resuscitation
CTG: fetal heartbeat, ferquent uterine activity
USS may be used to estimate fetal weight and exclude placenta previa but abruption may not be visible.
FBC, coagulation screen, cross-match. Catheterisation with hourly UO, regular FBC, Us&Es, CVP monitoring may be required in severe cases.
Features of major placental abruption
Maternal collapse
Coagulopathy
Fetal distress/demise
Woddy hard uterus
Poor UO or renal failure
Degree of vaginal loss is unhelpful
Mx of palcental abruption
Admit if pain and uterine tenderness. IV fluids. Steroids if gestation <34w. Blood transfusion. Opiate analagesia.
Delivery: depends on fetal state and gestation:
Fetal distress: emergency C-sec
No fetal distress but gestation is >37w induction of labour with amniotomy. Monitor mother and fetal distress.
If fetaus is dead: coagulopathy is also likely. Blood products given and labour induced.
If there is no fetal distress, pregnacny is preterms and abruption appears to be minor, steroids and pregnancy -> high risk .
PPH is the majory risk
What is bleeding of undetermined origin
APH small and painless without placenta praevia, may be difficult to find a cause.
USS little help.
What is vasa praevia
Occurs when fetal BS runs in the membranes in front of the presenting part.
rare but occur when the umbilical cord is attached to the membranes rather than the palcenta.
Can be detected on USS.
When membranes rupture, the vessel may rupture too.
Typical presentation is painless, moderate baginal bleeding at amniotomy or SROM which is accompanied by severe fetal distress.
NB for APH?
Cervical carcinoma can present in pregnancy.
If a cervical smear is overdue the woman with small recurrent or postcoital haemorrhage should undergo speculum exmaintions.
Definition of shoulder dystocia
Epidemiology.
Consequences?
When additional manoeuvres are required after normal downward traction has failed to deliver the shoulders after the head has delivered
1 in 200 deliveries
Characteristically results in Erb’s palsy (waiter’s tip) from excessive traction on the neck leading to damage to the brachial plexus.
Delay and unskilled attempts at delivery can be lethal (can be as short as 5 minutes from head to shoulder delivery)
Risk factors for dystocia
Large baby (>4kg although this only accounts for half of all cases)
Previous shoulder dystocia
Raised maternal BMI
Labour induction
Low height
Maternal diabetes
Instrumental delivery
Most cases considered unpreventable due to poor ability to predict and the prevention involves C-section
Mx of shoulder dystocia
Rapid and skilled intervention
Sequence of actions:
Because obstruction is at the pelvic inlet, excessive traction is useless.
Senior help.
Gentle downward traction
Legs are hyperextended onto the abdomen
Suprapubic pressure applied
This method works in 90% alternative methods if this fails involve internal manoeuvres necessitating episiotomy:
If the shoulders are transverese, pressure behind the anterior shoulder will rotate it to the widest diameter, combined with pressure on the anterior part of the posterior shoulder (Wood’s screw) can force delivery.
If this fails, posterior arm is grasped and by extension at the elbow the hand is brought down. The trunk will either follow or rotation of the body using the arm is performed.
Last resorts: symphysiotomy
Lateral replacement of the urethra with a metal catheter
Zavanelli maneuvre: replacement of the head and C-section, usually irreversible fetal damage has occured by this point.
McRobert’s maneuvre
Leg hyperextnension used in shoulder dystocia
Wood’s screw manoeuvre
Pressure on anterior shoulder and pressure on anterior part of posterior shoulder used in shoulder dystocia
Zavanelli manoeuvre
Reducing head back into uterus prior to c-sec in shoulder dystocia
Definition of cord prolapse
Occurs after ROM
Umbilical cord descends below the presenting part.
Untreated the cord will be compressed or go into spasm and the baby will rapidly become hypoxic.
1 in 500 deliveries
Risk factors for cord prolapse
Preterm labour
Breech presentation
Polyhydramnios
Abnormal lie
Twin pregnancy
(>50% occur at artificial amniotomy)
Dx of cord prolapse
Fetal heart rate abnormality
Vaginal palpation of the cord or its appearance at the introitus
Mx of cord prolapse
Presenting part must be prevented from compressing the cord: pushed up by the examining finger or tocolytics e.g. terbutaline are given.
If the cord is out of the introitus it should be kept warm and moist but not forced back inside.
Patient should go on all fours whilst preparation of delivery is undertaken.
C-sec usually used but instrumental vaginal delivery is appropriate when the cervix is fully dilated.
Def of amniotic fluid embolism
When liqupr enters the maternal circulation causing anaphylaxis with sudden dyspnoea, hypoxia and hypotension. Often accompanied by seizures and cardiac arrest.
Acute heart failure is evident.
Extremely rare but serious as often causes death.
If patient survives for >30mins she develops DIC, PO and ARDS.
Risk factors for amniotic fluid embolism
Membrane rupture, during labour, C-sec, TOP.
Multiple mild predisposing factor: strong contractions in the presence of polyhydramnios.
Prevention impossible
Mx of amniotic fluid emoblism
NB often confused with other causes of collapse and with eclampsia.
ABC resusc.
O2 and CVP monitoring.
Blooods for clotting, FBC, U&Es, cross match.
Blood and FFP will be required.
ICU admission.
Def: uterine rupture
Can be de novo or an old scar. Fetus is extruded. Uterus contracts and bleeds from rupture site causing acue fetal hypoxia and massive internal maternal haemorrhage.
Rupture of a lower trasnverse C-sec scar is usually less severe than others as the lower segment is not very vascular.
Occurs in 1/1500 pregnancies. and in 0.7% of women who attempt a vaginal delivery after a single previous lower C-sec.
Dx made from fetal HR abnormalities, constant lower abdo pain, vaginal bleeding, contraciton cessation, maternal collapse.
Risk factors for uterine rupture
Labours with a scarred uterus
Classical C-sec or deep myotomy.
Rupture before labour is rare
Neglected obstrcuted labour is rare in the West.
Congenital uterine abnormalities occasionally cause rupture before labour.
Preventive mesaures include avoidance of induction and caution when using oxytocin in women with previous C-sec.
Mx of uterine rupture
Maternal resus with IV fluid and bloods
Bloods taken fro clotting, Hb, X-match
Urgent laparotomy for fetal delivery and repair/removal of uterus.
Uterine rupture has a high recurrence rate
Def uterine inversion
When the fundus inverts into the uterine cavity.
Usually follows traction on the placenta and occurs in 1 in 20000 deliveries
Haemorrhage, pain and profound shock.
Brief immediate attempt to push the fundus up via the vagina.
If not, GA and replacement performed with hydrosstatic pressure of several litres of salin which is run past a clenched fist at the introitus.
Causes of epileptiform seizures in pregnant
Maternal epilepsy
Exlampsia
Hypoxia of any cause
Mx of epileptfiorm seizures in obstetrics
Assume pre-eclampsia, Mg sulphate
ABC
What is LA toxicity
Excessive doses or inadvertent IV doses of LA can cause transient cardiac, respiratoey and neurological consequences
What is the optimal initial management of cord prolapse in a fully equipped hospital setting?
When cord prolapse is diagnosed before full dilatation, assistance should be immediately called and preparations made for immediate birth in theatre. T
here are insufficient data to evaluate manual replacement of the prolapsed cord above the presenting part to allow continuation of labour. This practice is not recommended
. To prevent vasospasm, there should be minimal handling of loops of cord lying outside the vagina.
To prevent cord compression, it is recommended that the presenting part be elevated either manually or by filling the urinary bladder.
Cord compression can be further reduced by the mother adopting the knee–chest or left lateral (preferably with head down and pillow under the left hip) position.
Tocolysis can be considered while preparing for caesarean section if there are persistent fetal heart rate abnormalities after attempts to prevent compression mechanically, particularly when birth is likely to be delayed.
Although the measures described above are potentially useful during preparation for birth, they must not result in unnecessary delay.
What are the aims of antenatal care? (6)
Detect and manage pre-existing maternal disorders that may affect outcome of pregnancy
Prevent or detect and manage maternal complications of pregnancy
” fetal compications
Detect congenital fetal problems
Plan with mother the circumstancs of delivery to ensure maximum safety for the mother and baby
Provide education and advice regarding lifestyle and ‘minor’ conditions of pregnancy
Preconceptual care, components
Previous pregnancies: implications
Health check: better performed before conception
Rubella status
Strict preconceptual glucose control in diabetics to reduce the incidence of congenital abnormalities
Medication optimisation
Folic acid supplementation e.g. 0.4mg/day preconceptually.
Advice regarding smoking, ETOH, drugs
When is the booking visit
What is its purpose
Should be before 10 weeks gestation
To secreen for potential cxs that may arise during pregnancy: Risk assessment using Hx and Ex.
Decide about type and frequency of antenatal care: need to be constantly re-evaluation as the pregnancy proceeds.
Check pregnancy gestation and arrange prenatal screening
General health chec,
Impact of age on pregnancy risk
<17y/o >35y/o are at greater risk of obstetric and mediocal cxs.
Chromosomal abnormalities increase with age
Impact of past obstetric Hx on pregnancy risk
Many obstetric disorders have a small but significant recurrence rate
include: preterm labour, small for dates, IUGR, stillbirth, APH, PPH, some congenital abnromalities, rhesus disease, pre-eclampsia, GDM
Impact of gynae Hx on pregnancy risk
Hx of subferitility increases perinatal risk: IVF/augmentatin of fertilisation increases likelihood of multiple pregnancy.
Previous uterine surgery (e.g. myomectomy) may be an indication for elective C-section
Cervical smear Hx
Impact on PMHx on pregnancy risk
HTN, DM, autoimmune disease, Hbopathy, thromboembolic disease, CVD, R disease or other serios diseases are at an increased risk of pregancy problems.
Direct questions re: depression are useful
Impact of FHx on pregnancy risk
DM in first degree relative increases rsik of GDM
HTN, thromboembolic, autoimmune disease and pre-eclampsia are also familial
Examination at booking visist
General health and nutritional status
BMI
Baseline BP
Incidental disease may be detected e.g. breast carcinoma
Abdo examination: limited before third trimester. Uterus palpable from 12w. Fetal heart can be ausucltated at this point.
If no recent smear, usually performed 3 months post-natally.
Booking visit investigations and details.
USS: 11-13+6 to date using crown-rump length. Also detects multiple pregnancy and allows screening for nuchal translucency.
DS screen: nuchal translucency, beta-hCG and pregnancy-associated plasma protein A (PAPPA) = combined test
Bloods: FBC (?anaemia). Serum Abs (anti-D) to identify those at risk of intrauterine isoimmunisation. GGT (in those at risk, normally perforemd later in pregnancy). Syphillis test (VDRL). Rubella immunity checked (vaccination postnatally). HIV and HBV screening. Hb electrophoresis.
Screening for infections implicatd in preterm labour (e.g. Chlamydia, BV).
Urine MC+S because asymptomatic bacteruria in pregnancy can lead to pyelnephritis in (20%)
Urinalysis for glucose, protein and nitrites
Folic acid supplementation 0.4mg/d
Vit d supplementation 10 microg/d recommended for women >30BMI, SEA or afrocarribean origin or with low sunlight absoprtion.
Fe supplementation should not be routine
What is the calorific intake in pregnancy?
ETOH?
Smoking in pregnancy?
Dental?
Coitus?
Infection avodiance
Exercise?
Seatbelt?
2500
Avoided or <1 unit
Smoking cessation with nicotine replacement therapy
Dental cehck up advised
Coitus is not contraindicated unless: placenta praevia, or ROMed.
Listeriosis is avoided by drinking pasteurised milk and avoiding soft and blue cheese, pate and undercooked or partially cooked prepared foods. Salmonella avoided by cooking eggs and poultry well.
Eservices advised.
Above and below the bump.
What are the two care options for pregnancy in hte UK?
Communiy: core team of midwives. Women can be referred to hospital
Consultant-led care
Risk assessment for VTE should be considered
When is the anomaly USS?
20w: enables detection of most structural fetal abnormalities.
What are the USS screening for risk assesments and whena re they performed?
Doppler of the uterine arteries at 23w can be used as a screening test for IUGR and pre-eclampsia.
Not performed routinely but in htose at risk
What are the NICE recommended appts schedules for antenatal visits in pregnancy?
Uncomplicated: 10 for nulliparous. 7 for multiparous
More frequent visits are appropriate for many “high-risk” pregnancies.
What are the components of the examination in antenatal visits?
BP
Urine dip-> urine culture/analysis if abnormality found
Abdominal exam: lie, engagement (unimportant until 36w)
Fetal heart
What is the 16w visit in pregnancy for?
Results of screening tests for chromosomal abnormalities.
R/v of booking bloods.
18-21w purpose of visit
Anomaly scan
Repeat scan arranged at 32w if low-lying placenta
Purpose of 25w antenatal vist
Exclusion of early onset pre-eclampsia (only in nulliparous)
Purpose of 28w antenatal visit
Fundal height
FBC and Abs
GTT is perforemd if indicated
Anti-D given to rhesus-negative women
Purpose of 31w antenatal visit
Fundal height, R/v of bloods from 28w (nulliparous only)
Purpose of 36, 38, 40 antenatal visits
Fundal height measured
Fetal lie and presentation
Referral for external cephalic version if presentation if breech (ECV)
Pelvic examination inappropriate unless induction is complicated or there is suspicion of obstruction (and placenta praevia has been excluded)
Purpose of 41w antenatal visit
Fundal height measure and fetal lie and presentation checked
Membrane sweeping is offered as is induciton of labour by 42w.
Itching in pregnancy
Common
Scleare checked for jaundice and LFTs and bile acids assessed
NB although rare liver issue in pregnancy may bpresent with itching
Pelvic girdle pain in pregnancy
Mx
Formerly pubic symphysis dysfunction
Common and causes varying degrees of discomfort
PT, corsets, analgesics and even crutches may be used
Care with leg abduction required
Heartburn in pregnancy
Mx
Affects 70%, most marked in supine position
Extra pillows are helpful.
Diet modification.
Antacids can be used
Ranitidine in severe cases (NB pre-eclampsia can present with epigastric pain)
Backache in pregnancy
Mx
Universal and may cause sciatica
Most cases resolve after delivery
PT, advice on posture and lifting, a firm mattress and corset may all felp
Constipation in pregnancy
Common and exacerbated by oral Fe.
High fibre intake.
Stool softners can be used.
Oedema in pregnancy
Common, worsens towards the end (unreliable sign of pre-eclampsia).
Sudden increase warrants assessment and FU of BP and urinalyis.
Benign oedema is helped by raising feet.
Diuretics should not be given.
Leg cramps in pregnancy
Affects 30% of women.
Treatments unproven but NaCl, Ca salts or quinine may be tried
Cause of carpal tunnel syndrome in pregnancy
Mx
Due to fluid retention compressing the median nerve.
Seldom severe, usually temporary. Splinting of the wrists may help.
Vaginitis in pregnancy
DDue to candida infection
Common and difficult to treat
Itchy, non-offensive, white-grey discharge.
Imidazole vaginal pessaires (e.g. clotrimazole) can be used for symptomatic infection.
Tiredness in pregnancy
Common, NB often incorrectly attributed to anaemia.
Changse in weight in pregnancy
Gain 10-15kg
Changes in UT in pregnancy
Uterus increases weight from 50g-1000g
Muscle hypertrophy, increased blood flow and contractility.
Cervix softens and may start to efface late in third trimester
Changes in blood in pregnancy
50% increase in blood volume
Increased red cell mass
Decreased Hb
Increased WCC
Changes in CVs in pregnancy
CO: 40% increase
Peripheral resitance: 50% reduction
BP: falls in mid-regnancy.
Changes in lung in pregnancy
Tidal volume: 40% increase
No change in RR
Changes to
Renal
Gut
Thyroid in pregnacny
Renal blood flow: 40% increase in GFR so creatinine/urea decreased
Reduce motility: delayed gastric emptying and constipation
Enlargement of thyroid.
First trimester
Second
Third
w1-12
13-27
28-birth
Components of a Bishop score
Cut offs
Cervical position
Cervical consistency
Cervical effacement
Cervical dilation
Fetal station
<5- indicates labour unlikely to start without induction
>9- indicates htat labour will most likely commence spontaneously.
What is the epidemiology of breech presenation?
present in 25% at 28w.
Only occurs in 3% of babies near term
What are the different types of breech presentation?
Frank: hips flexed and knees fully extended
Footling: one or both feet come first with the bottom at a higher position (rare but carries a higher perinatal morbidity)
What are the risk factors for breech presentation?
Uterine malformations: fibroids
Placenta praevia
Poly/oligohydramnios
Fetal abnromality (e.g. CNS malformation, chromosomal disorders).
Prematurity (due to increased incidence earlier in gestation)
Mx of breech presentation
<36w
36w
If reamins breech
Fetaus may turn spontaneously.
ECV: success rate of around 60% (RCOG recommend ECV should be offered from 36w in nulliparous and 37 in parous)
Planned C-sec or vaginal
What information about C-sec and breech is important
Planned C-sec carries a reduced perinatal mortality and early neonatal morbidity for babies with a breech presentation at term compared with planned vaginal birth
There is no evidence that the long term health of babies with a breech presentation delivered at term is influenced by how the baby is born
Absolite contraindications of ECV
Indication for C-sec irrespective of fetal presentation (e.g. placenta praevia)
Severe oligohydramnios or ROM
Nonreassuring fetal monitoring test results
Hyperextended fetal head
Significant fetal or uterine anomaly
PLacental abruption
Multiple gestation (can be considered for the second twin after delivery of the first twin)
What are the relative contraindications of ECV?
Maternal HTN
Maternal obesity
fetal growth restriction
Oligohydramnios
Previous C-sec.
What differentiates clinically between cholestasis of pregnancy and acute fatty acid of pregnancy?
holestasis of pregnancy is characterised by severe pruritis, whereas acute fatty liver of pregnancy has predominantly non-specific symptoms (e.g. malaise, fatigue, nausea). With a normal FBC and viral screen a diagnosis of HELLP syndrome or viral hepatitis is unlikely.
Features of intrahepatic cholestasis of pregnancy (aka obstetric cholestatis)
Mx
Intrahepatic cholestasis of pregnancy: caused by impaired bile flow. Leads to build up of bile salts which can then deposit in the skin as well as the placenta.
Can be uncomfortable for mohter but may also cause sudden asphyxial events in fetus leading to anoxia and death.
pruritus: typically worse on palms, soles and abodmen
bilirubin < 100
occurs in 2nd and 3rd trimester
Increased risk of preterm birth
Mx: induction at 37w.
Ursodeoxycholic acid
Vit K supplementaiton
Features of acute fatty liver of pregnacny
Rare complication which may occure in third trimester or immediately following delivery
Abdo pain, N+V, headache, jaundice, hypoglycaemia, severe disease may result in pre-eclampsia
ALT typically elevated e.g. 500u/l
Mx: supportive care, stabilised: delivery is the definitive manageemtn
NB Gilbert’s and DJS may be exacerbated during pregnancy
What is the ovarian blood supply?
And the ligamental organisation?
From the ovarian artery which anastamoses with branches of the uterine artery in the broad ligament.
Overy lie the uretur in the ovarian fossa. Attached to the broad ligament by the mesovarium, the pelvic side wall by the infundibulopelvic ligament and to the uterus by the ovarian ligament
From which layer of the ovary does the most common carcinoma derive?
The outer cortex which is covered by germinal epithelium
What are the layers of the ovary?
Outer cortex: germinal epithelium
Inner medulla: connective tissue and bvs
Cortex contains the follicles and theca cells.
Whence is oestrogen secretion?
What can occur
Granulosa cells in the growing follicles and also by theca cells
Rare tumours of these cells secrete oestrogens.
What changes occur to the follicles during ovulation
Multiple enlarge every month under influence of FSH
Onle one reaches 20mm and ruptures in response to mid cycle LH surge
Collapsed follicle becomes a corpus luteum and continues to produce oestrogen and progesterone to maintain the endometrium.
If no implantation occurs the corpus luteum involutes and hormone levels decline.
If fertilisation occurs hCG from the trophoblast maintains the corpus luteum’s function and hormone production until 7-9w when the placenta takes over.
Follicular and lutein cysts result from persistence of these structures in nonpregnant women.
What are the symptoms of ovarian masses
Often silent and detected either when they are very large and cause abdominal distension or on USS.
Acute presentation is associated with “accidents”
What are the different types of ovarian cyst accidents?
Rupture of cyst into the peritoneal cavity.
Haemaorrhage into a cyst or peritoenal cavity
Torsion of the pedcile
What are the features of ovarian cyst rupture
Rupture of the cyst contents into the peritoneal cavity causes intense pain.
This is especially the cause with an endometrioma or dermoid cyst.
What are the features of haemorrhage of a cyst
Can occur into a cyst or the peritoneal cavity.
Often causes pain.
Peritoneal cavity haemorrhage can occasionally cause hypovolaemic shock
What are the features of torsion of the ovary?
Torsion of the pedicle (which is bulky due to the cyst) causes infarction of the ovary and tube and severe pain.
Sx and detorsion required urgently to save the ovary
What are the features of PCOS?
Causees oligomenorrhoea, hirsutism and subfertility.
Actually small multiple, poorly developed follicles rather than cysts
What is the most common gonadal dysgeneses?
Turner’s
Why are benign cysts classified with primary neoplasms of the ovary?
Because they may undrego malignant change
What are the three main groups of primary ovarian neoplasms?
Epithelial tumours
Germ cell tumours
Sex cord tumours
What are the most common ovarian masses premenopausally?
Follicular/lutein cysts
Dermoid cysts
Endometriomas
Benign epithelial tumour
What are the most common ovarian masses postmenopausally?
Benign epithelial tumour
Malignancy
Which group of women are epithelial tumours most commonly found in?
What are the features of epithelial tumours that make them unique?
Postmenopausal
Histology may demonstrate borderline malignancy where malignant histological features are seen without invasion. Such tumours may become frankly malignant and Sx is advised
How does the management of borderline epithelial cysts in younger women differ?
What is significant following removal of a cyst?
Close observation following removal of the cysts or affected ovary to retain fertility with close observation.
Recurrence as a borderline or invasive tumour can occur up to 20y later
What is the most common malignant ovarian neoplasm?
What is the benign form
Serous adenocarcinoma (50% of malignant neoplasms of the ovary) derives from the peithelial.
Serous cystadenoma
What proportion of ovarian malignancies is made up of mucinous adenocarcinoma?
What are the features?
10%
Mucinous cystadenoma can become very large and are less frequently malignant.
What is a rare borderline variant of the mucinous cystadenoma?
What happens?
What should be excluded?
Pseudomyxoma peritonei
Abdominal cavity fills with gelatinous mucin secretions.
Appendieal primary should be excluded.
What proportion of ovarian malignancies are accounted for by endometroid carcinomas?
25%
Similar histologically to endometrial carcinoma. with which it is associated in 20%
Which ovarian neoplasm has a particulaarly poor prognosis?
What proportion of ovarian malignancies are accounted for by this?
Clear cell carcinoma (epithelial tumours)
<10%
What are Brenner Tumours
Rare small and usually benign tumours of the ovarian epithelium
What are the relavent proprtions of the incidences of the following ovarian malignancies?
From which tissue layer do they arise
Serous adenocarcinoma
Mucinous adenocarcinoma
Endometroid carcinoma
Clear cell carcinoma
Epiethlium
50%
10%
25% (associated with endometrial carcinoma in 20% of cases)
<10%
Whence do germ cell tumours arise?
What are the different kingds of GCT?
From undifferentiated primordial germ cells of the gonad
What is a teratoma also known as?
What tissue do they arise from?
What are the features?
What is the malignant form?
Dermoid cyst
Undifferentiated primordial germs cells of the gonad.
Common benign tumours arising in young premenopasual women.
May contain fully differentiated tissue from all cell lines.
Commonly bilateral, seldom large, asymptomatic.
May rupture.
The solid teratoma
What is a dysgerminoma?
Features?
Female equivalent of the seminoma.
Very rare, most common ovarian malignancy in younger women.
Senesitive to RTx
What is the most common ovarian malignancy in younger women?
Dysgerminoma
Whence do sex cord tumours arise?
What are the different types?
From the stroma of the gona
Granulosa cell tumours
Tehcomas
Fibromas
What is a granulosa cell tumour?
Sex cord tumour.
Usually malignant but slow growing
Rare and found in postmenopausal women.
Stimulation of the endometrium may cause bleeding, endometrial hyperplasia, endometrial malignancy and precocious puberty (rarely in young girls)
How does a granulosa cell tumour cause endometrial changes?
What are these changes?
Secrete high livels of oestrogen and inhibin which can cause
bleeding
endometrial hyperplasia
malignancy
What is the tumour marker for granulosa cell tumours?
What is used for?
Serum inhibin
used to monitor for recurrence
What are the features of thecomas?
Rare
usually benign
Can secrete oestrogens or androgens
What are the features of fibromas?
Rare and benign tumours of the sex cord
Can cause Meig’s
What is Meig’s?
Ascites and usually right pleural effusions are found in conjunction with a small ovarian mass.
Effusion is benign and cured by removal of the mass
What is the proportion of ovarian masses are mets?
Where are the common sites?
10% of malignant ovarian masses
Breast
GIT
What are Krukenberg tumours
Mets to ovary from gut which contain “signet-ring” cells.
Primary malignancy may be difficult to detect and has very poor px
What are the features of endometriotic cysts
Endometriosis can cause altered blood to accumulate in “chocolates cysts”
In the ovary these are called endometriomas.
Rupture is painful though uncommon
“Tumour-like condition”
What are functional cysts?
Which causes more symptoms?
Follicular and lutein cysts are persistently enlarged follicles and CL respectively.
Only found in premenopausal women.
Protected against by OCP.
Lutein cysts.
“Tumour-like condition”
What is the Mx of functional cysts
Symptomatic treatment.
If asymptomatic, cyst is observed with serial USS.
Due to remote possibility of malignancy, if an apparent functional cyst >5mm persists beyond 2 months measure CA125 and consider laparoscopy to remove or drain the cyst
What is the 5 year survival rate of ovarian cancer
Why
<35%
Due to its silent nature
What is the epidemiology of ovarian malignacny
Rates increase with age
>80% in women >50
Highest age-specific incidence rates in 80-84
OCP use may be protective
What are the risk factors for ovarian malignancy?
Relate to number of ovulations:
Early menarche
Late menopause
Nulliparity
Familial: BRCA1 or 2 (also associated with breast), HNPCC (Lynch, lifetime incidence of bowel 80%) (if >2 relatives are affected the lifetime risk is 13%) if BRCA1: 50%.
What are the protective factors against ovarian malignancy?
Pregnancy
Lactation
Use of pill
Screening for ovarian cancer
Generally foer ealry malignant rather than premalignant
Those with BRCA1 and 2 are offered yearly TVUSS and CA125 or prophylactic SPO
What are the clinical features in terms of Hx in ovarian malignancy?
Vague/ absent, 70% present with Stage 3-4 disease
Warning signs;
Persistent abdominal distension (bloating)
Feeling full (early satiety) +/- loss of appetite
Pelvic or abdo pain
Increased urinary urgency and or frequency
Vaginal bleeding
Ask about breast/GI symptoms as ovarian mass may be met from these sites.
NB for overlap with IBS although this usually presents in younger women. Must exclude ovarian cancer in older women.
What are the clinical features in terms of Ex in ovarian malignancy?
Cachexia
Large abdo or pelvic mass (very large masses are less likely to be malignant)
Ascites
Breasts should be examined.
What are the features that make an ovarian mass more likely to be malignant?
Rapid growth >5cm
Ascietes
Advanced age
Bilateral masses
Solid or septate nature on USS
Increased vasculatiry
What is the normal spread of ovarian adenocarcinoma?
Usually spreads directly within the pelvis and abdomen (transcoelomic spread)
Lymapthic and histological spread can occur.
Staging is surgical and histological.
What are the stages of ovarian cancer
Stage 1: macroscopically confined to ovaries.
1a: one ovary affected, capsule intact
1b: both ovaries affected, capsule intact
1c: one/both, capsule not intact, or malignant cells in the abdominal cavity (ascites).
Stage 2: disease beyond ovaries, confined to pelvis
Stage 3: disease is beyond the pelvis but confined to the abdomen (frequent involvement of the omentum, small bowel and peritoneuM)
Stage 4: disease is beyond abdomen e.g. lungs or liver parenchyma
How is ovarian malignancy detected intiially
What is the cut off
What is the next action
CA125 should measured in women >50 with abdominal symptoms.
>35IU/mL
USS of abdomen or pelvis
If this dentifies ascites or pelvic or abdo mass, urgent referral to secondary care
How is ovarian cancer Dx established
What is a consideration in women <40?
CA125 measured if not already done so
Measure AFP and hCG as they are at increased risk of germ cell tumours.
How is the Risk of malignancy scored for women with ?ovarian cancer
What are the possible scores?
RMI= U x Mx CA125
U scored 1 point for: multilocular cysts, solid areas, metastases, ascites, bilateral lesions.
M menopausal status: 1= pre, 3= menopausal.
CA125= serum level.
What is the cut off of RMI?
>250-> referred to MDT
CT TAP may be performed, but staging usually established surgically.
What is the surgical Mx of ovarian Ca
Assess fitness for surgery
Midline laparatomy allows assessment of abdo and pelvis
Total hysterectomy with BSO and partial omentectomy perfromed.
Stage 1: sample retroperitoneal LNs
Stage 2 or greater they are all removed through block dissection.
Uterus and unilateral ovary may be preserved in younger women following laparoscopic Sx looking to maintain fertility however they require extensive f/u
What is the CTx Mx of ovarian Ca?
Confirmed tissue dx.
Very early, no CTx
Stage 1c: carboplatin
2-4 carboplatin +/- paclitaxel.
NB 2/3rds of women with initial response to CTx relapse within 2 years of completing treatment
RTx Mx of Ovarian Ca
Only used for dysgerminomas
What are the poor Pxic features of ovarian Ca?
What normally causes death?
Advanced stage
Poorly differentiated tumours
Clear Cell tumorus
Slow/poor response to CTx
Bowel obstruction or perf
Symptom control in palliative care of ovarian Ca
Pain?
N+V
Heavy vaginal bleeding
Ascites and bowel obstruction
Analgesic ladder, co-analgesics such as antidepressants steroids and cytotoxics may be used.
Antiemetics: anticholinergics, antihistamines, dopamine antagonists or 5HT-3 antags (ondanstrenon)
High dose progestogens may be helpful. RTx can be used.
Ascites: repeated paracentesis. Obstruction can be managed at home and resolution occurs in 1/3rd spontaneously. If partial: metoclopramide (pro-motility and antiemetic) + stool obstructers with enemas for constipation and a trial of dexmethasone.
Complete obstruction: cyclizine and odansetron for N+V with hyoscine for spasm. Surgical palliation indicated with acute, single-sight obstruction, may involve insertion of stents.
Terminal distress: good symptom control with anxiolytics and analgesics without oversedation
What is the definition of palliative care
Active total care of the patient whose disease is incurable
Increase QoL
Address symptoms
Mx of primary dysmenorrhoea
NSAIDs: mefanamic acid and ibuprofen effective in up to 80% ofr women.
Combined OCP= second line
What is the difference between 1o and 2o dysmenorhhoea
In primary dysmenorrhoea there is no underlying pelvic pathology. It affects up to 50% of menstruating women and usually appears within 1-2 years of the menarche. Excessive endometrial prostaglandin production is thought to be partially responsible.
Features
pain typically starts just before or within a few hours of the period starting suprapubic cramping pains which may radiate to the back or down the thigh
Secondary dysmenorrhoea typically develops many years after the menarche and is the result of an underlying pathology. In contrast to primary dysmenorrhoea the pain usually starts 3-4 days before the onset of the period. Causes include:
endometriosis
adenomyosis
pelvic inflammatory disease
intrauterine devices*
fibroids
What are the two methods of emergency contraception available in the UK?
Levonorgestrel (single does of a progesterone)
Ulipristal (progesterone R modulator)
What are the features of levonorgestrel?
should be taken as soon as possible - efficacy decreases with time
must be taken within 72 hrs of unprotected sexual intercourse (UPSI)*
single dose of levonorgestrel 1.5mg (a progesterone)
mode of action not fully understood - acts both to stop ovulation and inhibit implantation
84% effective is used within 72 hours of UPSI
levonorgestrel is safe and well tolerated. Disturbance of the current menstrual cycle is seen in a significant minority of women. Vomiting occurs in around 1%
if vomiting occurs within 2 hours then the dose should be repeated
can be used more than once in a menstrual cycle if clinically indicated
*may be offered after this period as long as the client is aware of reduced effectiveness and unlicensed indication
What are the features of Ulipristal?
a progesterone receptor modulator currently marketed as EllaOne. The primary mode of action is thought to be inhibition of ovulation
30mg oral dose taken as soon as possible, no later than 120 hours after intercourse
concomitant use with levonorgestrel is not recommended
may reduce the effectiveness of combined oral contraceptive pills and progesterone only pills
caution should be exercised in patients with severe asthma
repeated dosing within the same menstrual cycle is not recommended
breastfeeding should be delayed for one week after taking ulipristal. There are no such restrictions on the use of levonorgestrel
What is an alternative to the emergency contraceptive pill and its features?
Intrauterine device (IUD)
must be inserted within 5 days of UPSI, or
if a women presents after more than 5 days then an IUD may be fitted up to 5 days after the likely ovulation date
may inhibit fertilisation or implantation
prophylactic antibiotics may be given if the patient is considered to be at high-risk of sexually transmitted infection
is 99% effective regardless of where it is used in the cycle
may be left in-situ to provide long-term contraception. If the client wishes for the IUD to be removed it should be at least kept in until the next period
What are the high risk groups for pre-eclampsia?
What is the action taken?
NICE published guidance in 2010 on the management of hypertension in pregnancy. They also made recommendations on reducing the risk of hypertensive disorders developing in the first place. Women who are at high risk of developing pre-eclampsia should take aspirin 75mg od from 12 weeks until the birth of the baby. High risk groups include:
hypertensive disease during previous pregnancies
chronic kidney disease
autoimmune disorders such as SLE or antiphospholipid syndrome
type 1 or 2 diabetes mellitus
75mg Aspirin
What are the causes of urinary incontinence?
Causes
overactive bladder (OAB)/urge incontinence: due to detrusor over activity
stress incontinence: leaking small amounts when coughing or laughing
mixed incontinence: both urge and stress
overflow incontinence: due to bladder outlet obstruction, e.g. due to prostate enlargement
What is the initial investigation of UI?
bladder diaries should be completed for a minimum of 3 days
vaginal examination to exclude cystocele
urine dipstick and culture
What is the Mx of urinary incontinence?
Management depends on whether urge or stress UI is the predominant picture. If urge incontinence is predominant:
bladder retraining (lasts for a minimum of 6 weeks, the idea is to gradually increase the intervals between voiding)
bladder stabilising drugs: antimuscarinic is first-line
surgical management: e.g. sacral nerve stimulation
If stress incontinence is predominant:
pelvic floor muscle training (for a minimum of 3 months)
surgical procedures: e.g. retropubic mid-urethral tape procedures
D/c features of Candida
‘Cottage cheese’ discharge
Vulvitis
Itch
Trichomonas vaginalis
Offensive, yellow/green, frothy discharge
Vulvovaginitis
Strawberry cervix
Bacterial vaginosis
Offensive, thin, white/grey, ‘fishy’ discharge
What are the causes of vaginal discharge?
Common causes
physiological
Candida
Trichomonas vaginalis
bacterial vaginosis
Less common causes
Gonorrhoea
Chlamydia can cause a vaginal discharge although this is rarely the presenting symptoms
ectropion
foreign body
cervical cancer
What are acute causes of pelvic pain? (usually)
Ectopic pregnancy
UTI
Appendicitis
PID
Ovarian torsion
Miscarriage
Hx in ectopic pregnancy?
A typical history is a female with a history of 6-8 weeks amenorrhoea who presents with lower abdominal pain and later develops vaginal bleeding
Shoulder tip pain and cervical excitation may be seen
Urinary tract infection
Dysuria and frequency are common but women may experience suprapubic burning secondary to cystitis
Appendicitis
Pain initial in the central abdomen before localising to the right iliac fossa
Anorexia is common
Tachycardia, low-grade pyrexia, tenderness in RIF
Rovsing’s sign: more pain in RIF than LIF when palpating LIF
Pelvic inflammatory disease
Pelvic pain, fever, deep dyspareunia, vaginal discharge, dysuria and menstrual irregularities may occur
Cervical excitation may be found on examination
Ovarian torsion
Usually sudden onset unilateral lower abdominal pain. Onset may coincide with exercise.
Nausea and vomiting are common
Unilateral, tender adnexal mass on examination
Miscarriage
Vaginal bleeding and crampy lower abdominal pain following a period of amenorrhoea
Chronic causes of pelvic pain
Endometriosis
IBS
Ovarian Cyst
Urogenital prolapse
Endometriosis
Chronic pelvic pain
Dysmenorrhoea - pain often starts days before bleeding
Deep dyspareunia
Subfertility
Irritable bowel syndrome
Extremely common. The most consistent features are abdominal pain, bloating and change in bowel habit
Features such as lethargy, nausea, backache and bladder symptoms may also be present
Ovarian cyst
Unilateral dull ache which may be intermittent or only occur during intercourse. Torsion or rupture may lead to severe abdominal pain
Large cysts may cause abdominal swelling or pressure effects on the bladder
Urogenital prolapse
Seen in older women
Sensation of pressure, heaviness, ‘bearing-down’
Urinary symptoms: incontinence, frequency, urgency
N+V Mx in early pregnancy
Nausea and vomiting are very common in pregnancy, with 70-85% of pregnant women affected. Most cases are mild and do not require treatment, however anti-emetics may be considered if symptoms are persistent, severe and preventing daily activities. Suitable anti-emetics include cyclizine, metoclopramide, prochlorperazine, promethazine, chlorpromazine, domperidone and ondansetron. There is no evidence to suggest that any one of these drugs works better than another.
Mx of epilepsy in early pregnancy
Epilepsy affects 0.5% of pregnant women. It is a significant cause of maternal death, and so antiepileptic treatment is continued during pregnancy. However, antiepileptic drugs increase the risk of congenital abnormalities, particularly neural tube defects. Carbamazepine and lamotrigine are the safest drugs to prescribe, whereas sodium valproate should be avoided. This is because it is associated with a higher rate of congenital abnormalities and lower intelligence in children.
Preferred drug used in Mx of hyperthyroidism in early pregnancy?
Proplthiouricil
Mx of UTI in eraly pregnancy
Nitrofuratonin is preferred
Followed by trimethoprim and then cefalexin.
NB Nitrofurantoin should be avoided at term due to risk of neonatal haemolysis
Trimethoprim should be avoided during early pregnancy due to its action as a folic acid antagonist
What are the indications for induction of labour?
Indications
prolonged pregnancy, e.g. > 12 days after estimated date of delivery
prelabour premature rupture of the membranes, where labour does not start
diabetic mother > 38 weeks
rhesus incompatibility
What are the methods for induction of labour?
Method
membrane sweep
intravaginal prostaglandins
breaking of waters
oxytocin
A 19 year-old woman attends her GP for a repeat prescription of her combined oral contraceptive pill (COCP). Since starting it, she has been suffering from severe left sided headaches with changes in her vision before the headache begins. Clinical examination is normal. What is the most appropriate step in her management?
Stop the COCP and start treatment on a progesterone only contraceptive pill.
Immediately refer her to the emergency department
Refer her to a neurologist
Commence a different COCP
Stop the COCP and start an oestrogen only contraceptive pill
The woman is having migraines with aura - a condition that can increase using the COCP. Women who have migraine with aura should stop the pill immediately - this is because the oestrogen component of the COCP can increase the risk of the women having an ischaemic stroke. A progesterone-only contraceptive pill is therefore the only alternative contraceptive medication that can be prescribed, as the others have oestrogen.
What are the factors reducing HIV vertical transmission?
maternal antiretroviral therapy
mode of delivery (caesarean section)
neonatal antiretroviral therapy
infant feeding (bottle feeding)
ART in pregnancy
all pregnant women should be offered antiretroviral therapy regardless of whether they were taking it previously
if women are not currently taking antiretroviral therapy the RCOG recommend that it is commenced between 28 and 32 weeks of gestation and should be continued intrapartum. BHIVA recommend that antiretroviral therapy may be started at an earlier gestation depending upon the individual situati
Mode of delivery in pregnancy (HIV)
Mode of delivery
vaginal delivery is recommended if viral load is less than 50 copies/ml at 36 weeks, otherwise caesarian section is recommended
a zidovudine infusion should be started four hours before beginning the caesarean section
Neonatal antivrial therapy
zidovudine is usually administered orally to the neonate if maternal viral load is <50 copies/ml. Otherwise triple ART should be used. Therapy should be continued for 4-6 weeks.
A 28-year-old pregnant woman is seen at her booking appointment. Her obstetric history revealed she had pre-eclampsia in her last pregnancy. Which of the following medications should this patient be started on at 12-14 weeks gestation to reduce the risk of intrauterine growth retardation?
The following question tests the understanding of secondary prevention of women with pre-eclampsia. There is A level data showing that low-dose aspirin started at 12-14 weeks’ gestation is more effective than placebo at reducing occurrence of pre-eclampsia in women at high risk, reducing perinatal mortality and reducing the risk of babies being born small for gestational age . There is some evidence that low molecular weight heparin might reduce the placental insufficiency seen in pre-eclampsia, but long-term safety studies are not yet available. Labetalol and methyldopa are both common antihypertensive drugs used in the acute management of pre-eclampsia, however are not given prophylactically and do not reduce intrauterine growth retardation. Similarly to LMWH, unfractionated heparin has not been proven to prevent the development uteroplacental insufficiency.
NICE guidelines suggest that a woman who has a pre-labour rupture of membranes at term…
can either be offered induction of labour approximately 24 hours later or managed expectantly. Induction is often with vaginal PGE2.
What is the most appropriate first line investigation in a woman of reproductive age who has not conceived after 1 year of unprotected vaginal intervourse?
The most appropriate first line investigation in this patient is a day 21 progesterone. This is a non-invasive test and can tell you whether the patient is actually ovulating.
Both serum prolactin and thyroid function tests are not recommended unless patient’s have a specific reason for being tested i.e. a pituitary tumour or signs of overt thyroid disease.
What are the risks to the mother and foetus of VZV in pregnancy?
Risks to the mother
5 times greater risk of pneumonitis
Fetal varicella syndrome (FVS)
risk of FVS following maternal varicella exposure is around 1% if occurs before 20 weeks gestation
studies have shown a very small number of cases occurring between 20-28 weeks gestation and none following 28 weeks
features of FVS include skin scarring, eye defects (microphthalmia), limb hypoplasia, microcephaly and learning disabilities
Other risks to the fetus
shingles in infancy: 1-2% risk if maternal exposure in the second or third trimester
severe neonatal varicella: if mother develops rash between 5 days before and 2 days after birth there is a risk of neonatal varicella, which may be fatal to the newborn child in around 20% of cases
Mx of VZV exposure in pregnant women?
Management of chickenpox exposure
if there is any doubt about the mother previously having chickenpox maternal blood should be urgently checked for varicella antibodies
if the pregnant women is not immune to varicella she should be given varicella zoster immunoglobulin (VZIG) as soon as possible. RCOG and Greenbook guidelines suggest VZIG is effective up to 10 days post exposure
consensus guidelines suggest oral aciclovir should be given if pregnant women with chickenpox present within 24 hours of onset of the rash
Features of ectopic pregnancy
A typical history is a female with a history of 6-8 weeks amenorrhoea who presents with lower abdominal pain and later develops vaginal bleeding
lower abdominal pain: typically the first symptom. Pain is usually constant and may be unilateral. Due to tubal spasm
vaginal bleeding: usually less than a normal period, may be dark brown in colour
history of recent amenorrhoea: typically 6-8 weeks from start of last period; if longer (e.g. 10 wks) this suggest another causes e.g. inevitable abortion
peritoneal bleeding can cause shoulder tip pain and pain on defecation / urination
Examination findings
abdominal tenderness
cervical excitation (also known as cervical motion tenderness)
adnexal mass: NICE advise NOT to examine for an adnexal mass due to an increased risk of rupturing the pregnancy. A pelvic examination to check for cervical excitation is however recommended
Examination in ectopic pregnancy?
adnexal mass: NICE advise NOT to examine for an adnexal mass due to an increased risk of rupturing the pregnancy. A pelvic examination to check for cervical excitation is however recommended
What are the risk factors for endometrial carcinoma?
obesity
nulliparity
early menarche
late menopause
unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
diabetes mellitus
tamoxifen
polycystic ovarian syndrome
A 25-year-old woman presents 5 months after having dilation and curettage for a miscarriage. Since this procedure she has not had a period. A pregnancy test is negative. Hysteroscopy is performed which reveals the diagnosis.
Asherman’s syndrome, or intrauterine adhesions, may occur following dilation and curettage. This may prevent the endometrium responding to oestrogen as it normally would.
Ix in 2o amenorrhoea
exclude pregnancy with urinary or serum bHCG
gonadotrophins: low levels indicate a hypothalamic cause where as raised levels suggest an ovarian problem (e.g. Premature ovarian failure)
prolactin
androgen levels: raised levels may be seen in PCOS
oestradiol
thyroid function tests
Causes of secondary amenorrhoea (after excluding pregnancy)
hypothalamic amenorrhoea (e.g. Stress, excessive exercise)
polycystic ovarian syndrome (PCOS)
hyperprolactinaemia
premature ovarian failure
thyrotoxicosis*
Sheehan’s syndrome
Asherman’s syndrome (intrauterine adhesions)
Classification of tears following SVD
first degree: superficial damage with no muscle involvement
second degree: injury to the perineal muscle, but not involving the anal sphincter
third degree: injury to perineum involving the anal sphincter complex (external anal sphincter, EAS and internal anal sphincter, IAS):
3a: less than 50% of EAS thickness torn
3b: more than 50% of EAS thickness torn
3c: IAS torn
fourth degree: injury to perineum involving the anal sphincter complex (EAS and IAS) and rectal mucosa
Risk factors for perineal tears
Risk factors for perineal tears
primigravida
large babies
precipitant labour
shoulder dystocia
forceps delivery
Mx of mastitis
Mastitis affects around 1 in 10 breast feeding women. The BNF advises to treat ‘if systemically unwell, if nipple fissure present, if symptoms do not improve after 12-24 hours of effective milk removal of if culture indicates infection’. The first-line antibiotic is flucloxacillin for 10-14 days. Breast feeding or expressing should continue during treatment.
Referral to hospital for review by the surgical team is only appropriate if a breast abscess is suspected. This patient has no palpable lump therefore an abscess is unlikely.
Indications for oral antibiotics in mastitis
Rx
Infected nipple fissure not improving after 12-24h following effective milk removal
Breast milk culture positive
Fluclox for 10-14d
Erythromycin or clarithromycin if penallergic
Predisposing factors for candidiasis
diabetes mellitus
drugs: antibiotics, steroids
pregnancy
immunosuppression: HIV, iatrogenic
Mx of candidiasis
options include local or oral treatment
local treatments include clotrimazole pessary (e.g. clotrimazole 500mg PV stat)
oral treatments include itraconazole 200mg PO bd for 1 day or fluconazole 150mg PO stat
if pregnant then only local treatments (e.g. cream or pessaries) may be used - oral treatments are contraindicated
Causes of recurrent vaginal candidiasis
compliance with previous treatment should be checked
confirm initial diagnosis i.e. high vaginal swab, exclude differential diagnoses such as lichen sclerosus
exclude predisposing factors (see above)
consider the use of an induction-maintenance regime, with daily treatment for a week followed by maintenance treatment weekly for 6 months
Down Syndrome screening tests in pregnancy.
The combined test is recommended at 10-14 weeks gestation. It involves an ultrasound scan for nuchal translucency and a blood test for levels of Beta-human chorionic gonadotrophin (beta-hCG) and pregnancy associated plasma protein A (PAPP-A). In pregnancies with Down Syndrome, PAPP-A is low and beta-hCG raised.
If the window for the combined test was missed, at 14-20 gestation, the quadruple test will be offered. This involves a blood test for levels of alfa-fetoprotein (AFP), unconjugated oestriol, beta-hCG and inhibin A. In pregnancies with Down Syndrome, AFP and unconjugated oestriol are low and beta-hCG and inhibin A are raised.
Norethisterone 5 mg tds can be used as
a short-term option to rapidly stop heavy menstrual bleeding.
Draw the flow chart for the Mx of a woman presenting with menorrhagia
Mx of pregnant women with previous Hx of GBS
Group B streptococcus is a bacteria which is put of the natural gut flora and can colonise the vagina. About 50% of babies born to women who carry Group B streptococcus will become carriers themselves but less than 1% will be ill themselves. The largest risk factor for a baby developing Group B streptococcus growth is the mother having a previous baby who has grown it - the risk is increased by a factor of 10.
High risk women should be treated with intrapartum antibiotics, this reduces the risk of the baby developing Group B streptococcus. There is no need for antibiotics prior to labour. Having a vaginal or rectal swab will not change management as intrapartum antibiotics would still be recommended even if they were negative.
Women who have known GBS carrier status prior to this pregnancy, but have not had a baby with a GBS pregnancy there is not a requirement for IV antibiotics during labour unless another risk factor is present.
Offer intrapartum antibiotic prophylaxis using intravenous benzylpenicillin to prevent early-onset neonatal infection for women who have had:
a previous baby with an invasive group B streptococcal infection
group B streptococcal colonisation, bacteriuria or infection in the current pregnancy.
Intrapartum use of GBS for mother antibiotic choice
Benzylpenicllin
Clindamycin if penallergic
What is first choice empirical antibiotic for use in baby in ?GBS infection
IV benzylpenicillin and gentamicin
Risk factors for GBS infection?
Risk factors for Group B Streptococcus (GBS) infection:
prematurity
prolonged rupture of the membranes
previous sibling GBS infection
maternal pyrexia e.g. secondary to chorioamnionitis
Women found to have GBS infection in the antenatal period should be treated with intravenous antibiotics during labour. This has been shown to reduce early-onset GBS disease in the neonate
Extent of the vulva
Area of skin that stretches from the labie majora laterally to mons pubis anteriorly and the perieneum posteriorly. Overlaps the vestibule, the area between the labia minora and the hymen with surrounds the urethral and vaginal orifices
What is the epithelium of the vagina
What is found anteriorly?
Posteriorly?
Lymphatic drainage
Squamous epithelium
Bladder and urethra
Upper third is the pouch of Douglas, lower posterior wall close to the rectum
Most occurs via the femoral via the inguinal LNs and to the EIA nodes of the pelvis
What are the most common vulval symptoms
Pruritus
Soreness
Burning
Superficial dyspareunia
What are the causes of pruritus vulave?
Infections:
Candidiasis (+ vaginal d/c)
Vulval warts
Pubic lice/scabies
Dermatological disease:
Any condition esp eczma, psoriasis, lichen simplex, lichen sclerosus, lichen planus, contact dermatitis
Neoplasia:
Carcinoma
Premlaignant disease (vulval intraepithelial neiplasia
Features of lichen simplex
Ix
Mx
AKA chronic vulval dermatitis
Chronic inflammatory skin condition
Presents with severe intractable pruritus, especially at night
Labia majora typically inflamed and thicekend with hyper and hypopigmentation.
Symptoms can exacerbated by chemical or contact dermatitis
May be exacerbated by chemical or contact dermatitis. Linked to stress/ low Fe stores,
Vulval biopsy indicated if biopsy in doubt
Irritants such as soap should be avoided
Emollionts, moderately potent steroid creams and antihistamines
Features of liche planus
Affects skin anywhere on the body but particulalry mucosal surfaces
Presents with flat, papular purphlish lesions.
Can be erosive and more commonly assoicated with pain than pruritus
Treatment is with high-potency steroid creams:
potent – such as betamethasone dipropionate
very potent – such as clobetasol propionate
Topical calcineurin inhibitors may be used as second-line therapy
Systemic corticosteroids may be used for short periods in severe ongoing disease
Features of lichen sclerosus
Vulval epithelium is thin with loss of collagen.
May have autoimmune basis and thyroid disease and vitiligo may coexist.
Typically postmenopausal.
Causes severe pruritis which may be worse at night.
Uncontrollable scratiching may cause trauma. Pink-white papules with coalesce.
May cause inflammatory adhesions
Vulval carcinoma may develop in 5%.
Biopsy important to exclude carcinom.
treatment with ultra-potent topical steroids.
Vulvodynia
Vulvar dysaesthesiia (AKA)
Dx of exclusion.
No evidence of vulavl disease
Can be provoked or spontaneous and subdivided into to site: local or generalised.
Hx of UTI, OCP, psychosexual disorders.
Topical agents tend to be unhelpful. Oral
durgs e.g. amitriptyline or gabapentin used
Spontaneous generalised vulvar dysaesthesia
Burning pain that is more common in older patients
Vulvar dysaesthesia of the vestibule
Causes superficial dyspareunia or pain using tampons and is more common in younger women in whom introitus damage must be excluded.
Features of candidial infection of the vulva
Irritation and soreness of the vulva and anus rather than discharge.
topical or oral antifungal therapy may be necessary
What is the pathogeneis of Bartholin’s cyst/abscess
Blockage of ducts of the glands behind the labia manora causes cyst formation.
Infection may occur with Staphy or E Coli and an abscess forms.
Treatment is with incision and drainage and marsupialisation.
What is marsupialisation
Where an incision is sutured open to reduce the risk of re-formation
What are the features of introital damage
Commonly follows childbirth.
Overtightening, incorrect apposition at perineal repair or extensive scar tissue can cause superficial dyspareuina.
If the introitus is too tight, vaginal dilators or surgey can be used
What is Fenton’s repair?
The Fenton’s procedure (also called Fenton’s repair) is an operation to remove scar tissue and widen the vaginal opening when a woman experiences persistently painful sexual intercourse.
Health problems that may require a Fenton’s procedure include:
- Lichen planus of the vulva or vagina
- Lichen sclerosus of the vulva
- Previous surgery on the genitals that results in painful intercourse
- Childbirth tears
- Episiotomy complications
- Radiotherapy to the genitals
What is a common error in the consideration of vaginal cysts
Often mistaken for a prolapse
What is vaginal adenosis
When columnar epithelium is found in the normally squamous epithelium of the vaginal.
Occurs in women whose mothers received diethylstillboestrol in pregnancy
Can turn malignant (clear cell carcinoma of the vagina) although often spontaenously resolves.
Women with DES exposure in utero undergo annual screening by colposcopy.
What is VIN
What are the two types
Presence of atypical cells in the vulval epithelium
Usual: nearly all VIN is usual. Associated with HPV, CIN, smoking and chornic immunosuppression, Nay be mutlifocal and varied aappearaence. Associated with warty or basaloid SCC.
Differentiated: associated with lichen sclerosis, seen in older women, usually unfocal, linked to keratinisiing SCC of the vulva. Higher risk of progression to cancer thean for VIN.
Mx of VIN
Pruritus or pain common: emollients or mild topical steroid may help.
Gold standard is local surgical excision for symptomatic relief, to confirm histology and exclude invasive disease.
15% of women undergoing excision have unrecongised invasive disease. Therefore if conservative management is used, adequate biopsies must be taken.
VIN=
Vulval Intraepithelial Neoplasia
Epidemiology for carcinoma of the vulva
5% of genital tract cancers.
Most common >60y/o
What is the pathology of vulval carcinoma
95% are SCC.
Melanomas, BCC, adenocarcinomas and others accoutn for the rest.
Aetiology of vulval carcinoma
VIN is premalignant.
However it often arises de novo
Associated with lichen sclerosis, ummonsuppresion, smoking and paget’s disease of the vulva
What is paget’s disease of the vulva
Extramammary Paget’s disease (EMPD), also extramammary Paget disease, is a rare, slow-growing, usually noninvasive intraepithelial (in the skin)adenocarcinoma outside the mammary gland and includes Paget’s disease of the vulva and the extremely rare Paget’s disease of the penis
Hx in vulval carcinoma
Pruritus
Bleeding or d/c
Mass
Malignancy often presents late due to unnoticed lesions or embarrassment
Ex in carcinoma of vulva
Ulcer or mass
Most commonly on the labia majora or clitoris.
Inguinal LNs may be enlarged, hard and nodal
Spread of vulval carcinoma
Local and via LN-> superfiical then deep inguinal nodes-> femoral-> EIA.
Contralateral spread may occur
Staging is surigcal and histological
50% present with Stage 1 disease
Staging of vulval carcinoma
Stage 1:
a: Tumour confined to vulva/perineum, <2cm in size with stromal invasion <1mm. Negative nodes.
b: Tumour confined to vulva perineum, >2cm in size or with stromal invasion >1mm. negative nodes.
Stage 2: tumour of any size with adjacent spread, negative nodes.
Stage 3: tumour of any size with positive inguinofemoral nodes.
Stage 4: tumours invades upper urethra/vagina/rectum, bladder, bone or distant metastases (IVA vs IVB)
Ix of vulval carcinoma
Biopsy
Fitenss for surgery: CXR, EXG, FBC, U&E, X match
Treatment of vulval carcinoma
Stage 1a: wide local excision
For other stages: WLE and groin lymphadenectomy through skin-sparing incisions.
If the tumours doesn’t extende to within 2cm of midline unilateral excision of LNs has emerged. This has replaced the radical vulvectomy.
Cxs: wound break down, infection, lymphoaedma, lymphocyst formation and sexual and body image probelms.
RTx may be used for large tumours prior to Sx.
Px of vulval carcinoma
Many patients die from other age-related disease
Surival at Stage 1: >90%
Stage 3-4: 40%
Features of secondary vaginal carcinoma
Common and arises from local infiltration from cervix, endometrium or vulva or from metastatic spread from cervix, endometrium or GI tumours
Features of rpiamry carcinoma of the vagina
2% of all genital tract malignancies.
Affects oder women and is usually squamous.
Presents with bleeding or discharge and a mass or ulcer is evident.
Treatment with intravaginal RTx or radical surgery.
Survival at 5y: 50%
Features of clear cell adenocarcinoma of the vagina
Most common in the late teenage years.
Most are a rare Cx of DES prescription to mother during pregnacies to try to prevent miscarriage in 1950-70.
Radical surgery and RTx: good survival
What is the importance of infection in pregnancy?
Maternal illness may be worse e.g. varicella
Maternal complications: HIV infection implicated in pre-eclampsia
Preterm labour
Vertical transmission can cause miscarriage, can be teratogenic or damage developed organ or can cause serious infection in child.
Neurologic damage is more common in present of bacterial infrection
Antibiotic usage may be limited by potential adverse effects on foetus.
Features of CMV
Herpesvirus transmitted by personal contact.
Up to 1% of women develop CMV infection, usually subclinical in pregnancy.
Common cause of handicap and deafness
Fetal effects of CMV infection
Vertical transmission occurs in 40%
10% of infected neonates are symptomatic at birth with IUGR, pneumonia and thrombicytopenia.
Most of these will develop serious neurological sequelae: hearing, visual and mental impairment or die
Asympthomatic neonates are at risk of deafness.
Dx of CMV infection
USS abnromalities inconsitently present but include intracranial or hepatic calcification.
Most diagnoiesd using CMV testing.
CMV IgM remains positive a long time after infection, which could predate pregnancy, titres willl rise and IgG avidity will be low with recent infection.
If maternal infection confirmed: amniocentesis >6w post maternal infection will confirm or refute vertical trnsmission
Mx of CMV infection in pregnancy
Most infected neonates are not seriously affected.
Close surveillance for USS abnormlities and fetal blood sampling at 32w may help determine those at greatest risk for severe sequelae.
No prenatal treatment and termination may be offered.
Routine screening not advised.
Herpes simplex virus features
Responsible for most genital herpes
Less than 5% of pregnant women have a history of prior infection but man more have Abs
Fetal/neonatal effects of HSV
Not teratogenic.
Neonatal infeciton is rare but has a high mortality.
Vertical transmission occurs at vaginal delivery, particularly if vesicles are present.
More likely to occur in context of recent maternal infection because the fetus will not have maternal Abs (Risk >40%)
Dx of HSV infection
Cliinically and swabs are of little use
Mx of HSV infection in pregnancy
Referral to GU clinic
C-section for those delivering within 6w of primary attack and those with genital lesions from primary infection at time of infection.
Risk is less in recurrent herpes and they can have normal labour.
Daily aciclovir in late pregnancy may reduce the frequency of recurrences at term.
Exposed neonates are given IV aciclovir.
NB if there are CNS features in child at risk of HSV infection
LP shuld be performed
Aciclovir IV until infection excluded
Features of rubella in pregnancy
Congenital rublleea is very rare in UK due to immunisation
Effects of rubella on fetus
Maternal infection causes multiple fetal abnromalities including deafness, cardiac disease, eye problems, rmental retardation.
Probability and severity decreases with advancing gestation.
At 9w the risk is 90% if after 16w risk is very low.
Mx of rubella in pregnancy
If a non-immune woman develoips Rubella before 16w, TOP offered.
Screening routine at booking to identify those in need of vaccination after end of pregnancy.
Rubella vaccine is live and thus contraindicated in pregnancy.
Features of toxoplasmosis in pregnancy
Caused by T. gondii
Follows contact with cat faeces, soil or eating infected meat.
Infection in pregnancy occurs in 0.2% of women in UK but is more common in europe
Fetal/neonatal effects of toxoplasmosis
Fetal infection occurs in <50%
More common as pregnancy progresses.
Earlier infection leads to more severe sequelae: mental retardation, convulsions, spasiticities and visual impairment.
Dx of toxoplasmosis in pregnacny
USS may show hydrocephalus
Maternal infection diagnosed after IgM testing.
Flase positives and negatives are common
Can be diagnosed or excluded using amniocentesis after 20w.
Mx of toxoplasmosis
Health education to reduce risk of toxoplasmosis
Spiromycin intiated once maternal infection confirmed.
Additional combination therapy may be used following confirmation of vertical transmission although TOP may be requested.
Features of VZV
Chickenpox in pregnancy is rare but can cause severe maternal illness
Fetal/neonatal affects of VZV
Teratogenicity is a rare consequence of early pregnacny infection (which is immediately treated with oral aciclovir).
Maternal infection in the 4w preceding pregnancy may cause severe neonatal infection, this is most common if delivery occurs within 5d or 2d before maternal symptoms
Mx of VZV in pregnancy
Ig used to prevent and aciclovir to treat infection.
Pregnant women exposed are tested to confirm immunity. Ig recommended if they are non-immune
Aciclovir if infection occurs.
In late pregnancy neonates delivered in the risk period are given Ig. closely monitored and aciclovir if infection occurs.
What are the infections screened for in pregnancy
Asymptomatic bacturia: MSU
Chlamydia (<25y/o)
HBV
HIV
Rubella
Syphillis
Why should parvovirus B19 be tested for if ?Rubella in pregnancy?
As they are clinically indistinguishable.
How to treat pain or fever in pregnancy
Paracetamol
Ibuporfen may be considered but should not be used beyoind 27w gestation.
Features of parvovirus B19 infection
Infects 0.26% of pregnant women and more during epidemics
Slapped cheek is calssic but many have arthralgia or are asymptomatic
Fetal/neonatal effects of B19
Virus suppresses fetal erythropoiesis causing anaemia and variable degrees of thrombocytopenia
Fetal death occurs in 10% of pregnancies usually before 20w
Dx of B19
Where materanl exposure or syymtpoms have occurred maternal IgM testing will prompt fetal surveillance
Anaemia is detectable on USS as increased blood flow velocity in the fetal middle cerebral arteral and subsequently as oedema (fetal hydrops) from fetal heart failure.
Maternal testing may also follow identification hydrops
Hydrops and anaemia spontaneously resolves in 50%
Mx of B19
Mothers infected are regulalry sacanned
Where hydrops is detected, in utero transfusion is given is this is severe.
Evidence of severe disease being associated with neurological damage
Features of GBS infection in pregnancy
Caused by carriage of Streptococcus agalactiae which is asymptomatic in about 25% of pregnant women
Neonatal effects of GBS
The fetus can be infected during labour after ROM. Most commmon in pre term labour or PROM.
Maternal fever
Early onset GBS occurs in 1 in 500 neonates. Causes severe illness and has a 6% mortality in term and 18% mortality in preterm.
IV benzyl can prevent vertical transmission
Risk factors for GBS transmission
Previously affected neonate
Positive urinary culture for GBS
Preterm labour
ROM >18h
Maternal fever in labour
Treatment is usual for incidental GBS carriage.
Strategy 1 vs Strategy 2 for GBS
Strategy 1= treatment based on RFs
Strategy 2: screening with vaginal and rectal swabs at 35-37w
Treat with IV benzlypenicillin in labour if swabs positive or RFs present
Features of HBV in pregnancy
Persitent HBV infeciton presint in 1% of pregnant women up to 25% in those from Asia and Africa.
Degree of infectivity depends on Ab status. HBsAb are immunologically cured and of low infectivity.
Those with surface Ag but not Ab and those with E Ag are more infectious
Neonatal effects of HBV infection
Vertical transmission occurs at delivery.
90% of infected neonates become chronic carriers compared to 10% of adults
Mx of HBV infection
Neonatal immunisation reduces the risk of infection by over 90%.
Maternal screening is routine in
Offer tenofovir disoproxil to women with HBV DNA greater than 107 IU/ml in the third trimester to reduce the risk of transmission of HBV to the baby UK
Advise women that there is no risk of transmitting HBV to their babies through breastfeeding if guidance on hepatitis B immunisation has been followed, and that they may continue antiviral treatment while they are breastfeeding.
Maternal effects of HIV in pregnancy
Does not hasten progression to AIDS
Increased incidence of pre-eclampsia (may be increased by ARTs)
Gestational diabetes may be more commmon
Neonatal/fetal effects of HIV
Stillbirth, pre-eclampsia, IUGR and prematurity more problem
Congenital abnormalities aren’t and ARTs not teratogenic
NB Folic acid antagonists may be prescribed to HIV infected women.
The most important risk is of vertical transmission, beyond 36w, intrapartum or during breastfeedings.
25% of infected neonates develop AIDS by 1y, 40% will develop AIDS by 5y
Mx of HIV in pregnancy
HIV +ve women should be managed in conjunction with their physician and have regular CD4 and viral load tests.
Prophylaxis against PCP if low CD4
Drug toxicity monitored with LFT, RFT, Hb and blood glucose.
Ix for genital tract infections.
HAART including zidovudine which reduces viraemia and maternal disease and should be continued throughout pregnancy and delivery.
Neonate treated for the first 6w.
Therapy in women not already taking HAARTs is usally started at 28w.
C-section
Reduces vertical transmission to <1%
Features of GAS
Traditionally responsible for puerperal sepsis.
Most common bacterium associated with maternal death in which sepsis is the leading cause (50%).
Caused by strep pyogenes, NB sore throat.
Infection during as opposed to after pregnancy is usally from children.
Chorioamnionitis. abdo pain, diarrhoea and severe sepsis may ensue.
Infected fetus usually dies in utero
Early recognition, culture and high dose antibiotics and ITU required in severe cases..
IFV in pregnancy
Immunisation recommended
Oseltamivir and zanamivir
Admit esp if respiratory symptoms
Syphillis in pregnancy
Active disease in pregnacny usually causes miscarriage, severe congenital disease or stillbirth
Benzylpenicillin will prevent but not reverse fetal damage.
VDRL used for screening/ PCR
Implications of TB in pregnancy
Tuberculin testing is safe
BCG is live and contraindicated.
Dx in late pregnancy is associated with prematurity and IUGR.
Treatment with first line drugs and vitamin B6 is safe in pregnancy
Streptomycin is contraindicated
Implications of HCV infection in pregnancy
Vertical transmission occurs in 6% and is increased by HIV coinfection and high viral load.
Infected neonates are prone to chronic hepatitis.
C-sec doesn’t reduce vertical transmission.
Screening restricted to high risk groups
Maternal cxs of malaria infection
Severe anaemia and other problems are more common
Fetal cxs of malaria
IUGR and stillbirth are more common
Congenital malaria complicates 1% of affected pregnancies
Artemisin combination therapy appears safe.
Intermittent preventative treatment of 2 dosease at least a month apart can prevent maternal and neonatal infection
Where is L monocytogenes found?
What does it cause?
Dx?
Prevention
Gram negative bacillus found in pates, soft cheeses and prepacked meals
Causes nonspecific febrile illness.
If bacteraemia occurs in pregnancy then a potentially fatal infection of the fetus may occur.
Blood cultures
Avoidance of high risk food.
What are the implications of chlamydia/gonorrhoea infection in the neonate
Associated with preterm labour and neonatal conjunctivitis.
Treatment of of chlamydia in pregnancy?
azithromycin or erythromycin.
NB tetracycline causes fetal tooth discolouration
Treatment of gonorrhoea in pregnancy
Cephalosporins due to high prevalence of penicllin resistance
Most common causes of BV
Implications in pregnancy
Mx
Gardnerella vaginalis and mycoplasma hominis
Preter, labour and late miscarriage more common
Screning and treatment with oral clindamycin reduces the risk of preterm birth.
Anatomy and function of the female lower UT system
Voluntary control of urine release achieved by the bladder and urethra
Normal function of the filling phase relies upon adequate bladder capacity and competent urethral sphincter.
Normal function of the voiding phase is dependant upon detrusor contractility and coordinated urethral relaxation.
Bladder has a smooth muscle wall: detrusor muscle
Can store around 500mL or urine although first urge to void is at 200mL.
Drained by the urethra which is 4cm long and has a muscular wall and external orifice in the vestibule
Nervous control of the bladder
PNS: aids voiding
SNS: prevent
Afferent fibres respond to bladder wall distension
Effeerent PNS bass back to the detrusor muscle and cause contraction.
Efferent SNS fibres also pass to the detrusor and are inhibted.
This is the micturition reflex and is controlled at the level of the pons.
The cerebral cortex modulates this through relaxation or contraction of the pelvic floor and the striated muscle of the urethra
What are the factors that influence continence.
Prssure in the urethra being greater than in hte bladder.
Bladder pressure is influenced by detrusor pressure and intra-abdominal pressure.
Urethral pressure is influenced by the inherent urethral muscle tone and by external pressure (pelvic floor and intra-abdominal pressure).
The detrusor muscle is expandable, as bladder fills there is no increase in pressure.
Increases in abdominal pressure are transmitted equally to the bladder and upper urethra.
Therefore coughing does not normally lead to urinary incontinence.
When does micturition occur
When bladder pressure exceeds urethral pressure.
Achieved volunterily by simultaenous drop in urethral pressure (partly due to pelvic floor relaxation) and in bladder pressure due to detrusor contraction.
What are the two main causes of female incontinence?
Uncontrolled increases in detrusor pressure
Increased intra-abdominal pressure transmitted to bladder but not urethra
Rarer causes include urine bypassing the sphincter through a fistula
Or pressure overwhelming the sphincter due to overfilling of thbladder due to neurogenic causes
Or outflow obstruction leading to overflow incontiinece
What are the implications of uncontrolled increases in detrusor pressure
Most common cause
Increased bladder pressure beyond that of the normal urethra due to
OAB or urinary urge incontinence (previously called detrusor instability) i
What are the implications and cause of increased intra-abdominal pressure transmission to the bladder but not the urethra?
Incontininece, normally as a consequence of the urethral neck slipping from the abdomen.
Bladder pressure therefore exceeds urethral pressure when intra-abdominal pressure is raised.
This is most commonly caused by urinary stress incontince
What are hte common urinary symptoms?
Incontinence
Daytime frequency
Nocturia
Nocturnal enuresis
Urgency
Bladder pain
Urethral pain
Dysuria
Haematuria
What is urinary incontinence?
The complaint of involuntary urinary leakage wihich can be divided into stress incontinence and urge incontinence.
What is daytime frequency?
Normal?
Number of times a women voids during waking hours
Normall 4-7
Increased daytime frequency defined by patients perception
What is nocturia
Having to wake at night one or more times to void
<70y/o >1 per night= abnormal
What is nocturnal enuresis
Urinary incontinence during sleep
What is urgency?
Sudden compelling desire to pass urine, which is difficult to deter.
Most frequently secondary to detrusor overactivity
Inflammatory bladder conditions may also present with this
What is bladder pain and where is it typiically felt?
Supra or retropubic.
Pain occurs with bladder filling and is relieved by emptying it.
Pain is indicative of an intravesical pathology such as interstitial cystitis or malignancy
What is dysuria?
Pain felt in the bladder or urethra on passing urine, most frequently associated with UTI
What are the features of urine dipstick tests?
Blood, glucose, protein, leucocytes and nitrites
Nitrites suggestive of infection, if +ve MCS
Glycosuria suggests diabetes
Haematuria suggests bladder carcinoma or calculi
What is a urine diary
When a patient keeps a record for a week of the time and volume of fluid intake and micturition
What is the use of postmicturition ultrasound or catheterisation
Exclude chornic urinary retention
What is cystometry
Directly measures via a catheter, the pressure in the bladder while the bladder is filled and provoked with coughing.
A pressure transducer also placed in vagina or rectum to measure abdominal pressuor.
How can true detrusor pressure by caclulated?
Subtraction of the abdominal pressure from the vescile pressure.
Should not normally alter with filling or provocation
If urinary leaking occurs with coughing in the absence of detrusor contraciton what is the likely diagnosis?
Urodynamic stress incontinence
What is the diagnosis if an involuntary detrusor contraction occurs?
Detrusor overactivity
What is the use of ultrasonography in investigation of the urinary tract
Excludes incomplete bladder emptying.
Checks for congenital abnromalities or abnormalities of the kidneys
What is the use of CT urogram?
With the use of contrast the integrity and route of the uretur is examined
What is the methylene dye test?
BLue dye is instilled into the bladder, leakage from places other than the urether i.e. fistulae can be seen
What is the definition of urinary stress incontinence?
Whendoes it become urodynamic stress incontinence
What is the most common cause
Complaint of involuntary leakage of urine on effort or exertion, on sneezing or coughing.
Once it has been confirmed by urodynamic studies
As a result of urethral sphincter weakness, can only be made with certainty after cystometry.
What proportion of female incontinence is caused by stress incontinence?
50%
Occurs to verying degress in more than 10% of women
What are the causes of stress incontinence?
Pregnancy and vaginal delivery
Esp: prolonged labour, forceps delivery
Obestity and age.
Prolapse commonly exists but is not always related.
Previous hysterectomy (when indication was not for prolapse or urianry symptoms) may predispose to USI
What is the mechanism of stress incontinence
Increase in intra-abdominal pressure, normally the bladder neck is equally compressed and its pressure rises so the P difference remains unchanged.
If the bladder neck has slipped below the pelvic floor because its supports are weak it will not be compressed.
If the rest of the urethra are unable to compensate the bladder pressure exceeds urethral pressure and incontinence results.
Hx in stress incontinence
Disruption of patients life
Stress incontinence predominantes, may also complain of frequency, urgency or urge incontinence.
It is important to have the patient prioritise her symptoms as treatment for USI vs OAB differs.
Faecal incontinence may coexist (perineal tear during childbirth)
Ex in Stress incontinence
Sim’s speculum, often but not invariable reveals a cystocoele or urethrocoele.
Leakage of urine with coughing may be seen.
Abdo palpation to exclude bladder distension.
Ix in stress incontinence
Urine dipstick
Bladder diaries
Can measure post-void residual volume by bladder scan
Try conservative management before:
Cystometry is required to exclude overactive bladder is considered or if overactive bladder symptoms fail to respond to medical treatment
UTIs, MCS and antibiotics
Positive for leucocytes and nitrites with symtpoms; send an MSU for MCS and start empirical antibitotics.
Symptomatic and negative test for leucoytes or nitrites send an MSU for MCS and consider empirical antibiotics
If asymptomatic with postivie L and N, do not offer antibiotics without the results of MSU
If asymptomatic and negative for either L or N do not send for MCS as unlikely UTI
Mx of stress urinary incontinence
Conservative:
Modification of fluid intake
Lose weight if obese
Cause of chronic cough can be reduced e.g. smoking.
1st line Pelvic floor muscle training
Medical:
[Duloxetine (not routinely used as second line treatment unless woman prefers not to have surgery]
2nd line Sxical:
Considered when conservative measures have failed and woman’s QoL is being signficantly impact.
Need to be clear that USI is the cause
Mid-urethral sling using tension free tape and trans-obturator baginal tape are first line with cure rates up to 90%
If sx fails, artifical urinary sphincter may be considered.
What is duloxetine and its adverse effects
SNRI that enhances urethral striated sphincter activity
Associated with significant and dose-dependant reduction in frequency of incontinence episodes.
Can cause nausea, dyspepsia, dry mouth, dizziness, insomnia or drowsiness
What are the Cxs of surgery for USI?
Bladder perforation
Postoperative voiding difficulty
Bleeding
Infection
de novo detrusor overactivty and suture or mesh erosion
What is TVT?
Tension-free vaginal tape: synthetic polypropylene tape placed in a U-shape under the midurethra ander LA or GA, tension adjusted as woman coughs
Cystouerthroscopy is performed to ensure there has been no damage to bladder or urethra
What is TOT
Transobturator tape
Similar to TVT with different insertion methd (via the transobturator foramen)
Reduced risk of bladder perf as retropubic space isn’t entered.
What is injectable periurethral bulking?
Injection of bulking agents for the treatment of USI. Has a low immediate success rate but low morbidity so may be appropriate in patients where surgery has failed or very elderly patients.
What is the difference between USI and stress incontinence?
Stress incontinence is a symptom
USI is a disorder diagnosed only following cystometry
Def OAB?
Urgency with or without urge incontinence, usually with frequency or nocturia in the absence of proven infection.
What is detrusor overactivity?
Urodynamic diagnosis characterised by involuntary detrusor contractions during the filling phase which may be spontaenous or provoked by coughing.
What is the epidemiology of OAB
causes 35% of female incontinence
Aetiology of OAB
Can follow operations for USI in which case it may be caused by bladder neck obstruction.
May occasionally occur in hte context of detrusor overactivity occuring the presence of a neuropathy e.g. MS or SC injury
Mechanism of incontinence in OAB
Detrudor contraction normally felt as urgency. If strong enough it causes the bladder pressure to overcome the urethral pressure and the patient leaks= urge incontinence.
Can occur spontaneously or with provocation e.g. rise in IAP.
Hx in OAB
Urgency and urge incontinence
Frequency
Nocturia
Stress incontinence also common
Some patients leak at night or at orgasm
Hx of childhood enuresis is common
Faecal urgency
Ex in OAB
often normal but an incidental cystocoele may be present
Ix in OAB
Urine dip
Urine diary: frequent passage of small volumes of urine, particularly at night and may show high intake of caffeine containing drinks.
After lifetyle changes and trial of Rx, cystometry
Mx of OAB
Lifestlye changes:
Reduce fluid intake, obesity, avoiding caffeine, drugs that alter bladder function such as diuretic and antipsychotics should be reviewed.
Conservative:
1st line Bladder training lasting a minimum of 6 weeks
Medical:
Muscarinic antagonists
2nd line: Oxybutynin or toiterodine or darifenacin, offer durg with lowest acquisition cost
3rd line: oestrogens, mirabegron for symptomatic control
Sxical (only after cystometry):
Botulinum toxin injection
Percutnaeous nerve stimulation
Clam augmentation ileocystoplasty is used only for very severe and resistant symptoms, woman has to be willing to self catheterise
Urinary diversion (last ditch)
Anticholinergics MOA in OAB
Adverse effects
Suppress detrusor overactivity
Block muscarinic receptors that mediate detrusor smooth-muscle contraction relaxing the detrusor muscle
Dry mouth, dizziness (oxybutynin), constipation, blurred vision, drosiness and dizziness. Have also been known to induce delerium
MOA of oestrogens in OAB
Many women develop bladder filling symptoms after menopause
Improves symptoms of vaginal atrophy.
Can reduce symptoms of urgency, urge incontinence, frequency and notcuria
Botulinum A MOA in OAB
Cxs
Blocks NMJ transmission causing weakness
Injected cystoscopicall into the detrusor muscles with sparing of the trigonium.
Lasts 6m on average.
Voiding dysfunction and urinary retention
Features of neuromodulation and sacral nerve stimulation
Continuous stimulation of hte S3 nerve root via an electrical pulse generator improves the ability to suppress detrusor contractions
Causes of urgency and frequency
UTI
Bladder pathology
Pelvic mass
Overactive bladder
USI
What is Mixed incontinence
Combination of USI and OAB
Dx made at cytometry
Most bothersome symptom treated first
Def acute urinary intention
Features
Patient unable to pass urine for 12h or more.
Catheterisation producing as much or more urine than bladder capacity
Painful unless due to epidural anaesthesia or failure of the afferent pathway
Causes of acute urinary retention
Mx
Childbirth: epidural, vulval or perineal pain
Sx
Drugs such as anticholinergics
Retroverted gravid uterus
Pelvic mass
Neurological disease
Catheterisation for 48h whilst cause is treated
Features of chronic retention and urinary overflow
1% of incontinence
Bladder overdistension eventually causes overflow
Can be due to urethral obstruction or detrusor inactivity
Pelvic masses and incontinence sx are the most common causes of urethral obstruction
Autonomic neuropathies e.g. DM or previous overdistension of the bladder can cause detrusor inactivity.
Presentation may mimic stress incontinence or loss may be continuous
Examination reveals a distended non-tender bladder
Dx with USS or catheter after micturition
Features of painful bladder syndrome and interstitial cystitis
PBS= suprapubic pain due to bladder filling accompanied by other symptoms e.g. frequency in the absence of UTI
Dx of interstital cystitis reserved for pateitns with painful bladder who have characteristic cystoscopic and histological features.
Treatments include dietary modificatiion, bladder training, TCAs, analgesics and intravesical drug infusion
What are the most common fistulae causing incontinence
Vesicovaginal
Urethrovaginal
Commonly as a result of obstructed labour in the developing world, in West normally due to Sx, RTx or Ca.
Ix with CTU or cystoscopy.
Sx often required
Name that fistula!
- urethrovaginal
- vesicovaginal
- vesicouterine
- ureterovaginal
What are the cut offs for anaemia in pregnancy?
Anaemia in pregnancy is defined using different cut off values than in non-pregnant women and varies according to trimester. British Committee for Standards in Haematology (BCSH) guidance gives the following values:
first trimester Hb less than 110 g/l
second/third trimester Hb less than 105 g/l
postpartum Hb less than 100 g/l
What are the management options for anaemia in pregnancy?
Royal College of Obstetricians and Gynaecologists (RCOG) guidelines advise for normocytic or microcytic anaemia a trial of oral iron should be considered as the first step, and further investigations only required if no rise in haemaglobin after 2 weeks.
Parenteral iron is only indicated if oral iron is not tolerated, absorbed, patient is not compliant or they are near term and there is insufficient time for oral iron to be effective.
Blood transfusion is inappropriate at a slighlty low level of haemoglobin without active bleeding.
Define placental abruption
Epidemiology
Placental abruption describes separation of a normally sited placenta from the uterine wall, resulting in maternal haemorrhage into the intervening space
1/200 pregnancies
What are the associated factors for placental abruption?
Cause - not known but associated factors:
proteinuric hypertension
multiparity
maternal trauma
increasing maternal age
What are the clinical features of placental abruption
Clinical features
shock out of keeping with visible loss
pain constant
tender, tense uterus
normal lie and presentation
fetal heart: absent/distressed
coagulation problems
beware pre-eclampsia, DIC, anuria
Presents with sudden abdominal pain in the third trimester.
On examination the mother can be seen to be in extreme pain and cold to touch.
Bleeding is present in 80% of cases.
Absence of visible bleeding does not rule out this diagnosis.
Risk factors include: maternal hypertension (common), cocaine, trauma, uterine overdistension, tobacco and previous placental abruption.
What are the causative organisms for PID?
Causative organisms
Chlamydia trachomatis - the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis
What are the features of PID?
Features
lower abdominal pain
fever
deep dyspareunia
dysuria and menstrual irregularities may occur
vaginal or cervical discharge
cervical excitation
Ix of PID
screen for Chlamydia and Gonorrhoea
Mx of PID
due to the difficulty in making an accurate diagnosis, and the potential complications of untreated PID, consensus guidelines recommend having a low threshold for treatment
oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole
RCOG guidelines suggest that in mild cases of PID intrauterine contraceptive devices may be left in. The more recent BASHH guidelines suggest that the evidence is limited but that ‘ Removal of the IUD should be considered and may be associated with better short term clinical outcomes’
Cxs of PID
Complications
infertility - the risk may be as high as 10-20% after a single episode
chronic pelvic pain
ectopic pregnancy
Def PID
Pelvic inflammatory disease (PID) is a term used to describe infection and inflammation of the female pelvic organs including the uterus, fallopian tubes, ovaries and the surrounding peritoneum. It is usually the result of ascending infection from the endocervix
What are the major causes of bleeding in the 1st trimester?
Spontaneous abortion
Ectopic pregnancy
Hydatidiform mole
Causes of bleeding in 2nd trimester?
Spontaneous abortion
Hydatidiform mole
Placental abruption
Causes of bleeding in 3rd trimester?
Bloody show
Placental abruption
Placenta praevia
Vasa praevia
Hydatidiform mole features
Typically bleeding in first or early second trimester associated with exaggerated symptoms of pregnancy e.g. hyperemesis. The uterus may be large for dates and serum hCG is very high
Features of placenta praevia
Vaginal bleeding, no pain. Non-tender uterus* but lie and presentation may be abnormal
*vaginal examination should not be performed in primary care for suspected antepartum haemorrhage - women with placenta praevia may haemorrhage
Features of vasa praevia
Rupture of membranes followed immediately by vaginal bleeding. Fetal bradycardia is classically seen
What are indications for gynae referral in hyperemesis gravidarum?
Failure of oral antiemetics to control symptoms, ketonuria and weight loss (>5% of pre pregnancy body weight) are all reasons to refer a woman to gynaecology for urgent assessment and intravenous fluids. It is particularly important to keep a low threshold for referral if the woman has a concurrent condition which may be affected by prolonged nausea and vomiting (for example diabetes).
Def: hyperemesis gravidarum
Hyperemesis gravidarum describes excessive vomiting during pregnancy. It occurs in around 1% of pregnancies and is thought to be related to raised beta hCG levels. Hyperemesis gravidarum is most common between 8 and 12 weeks but may persist up to 20 weeks*.
*and in very rare cases beyond 20 weeks
Cxs of hyperemesis gravidarum
Wernicke’s encephalopathy
Mallory-Weiss tear
central pontine myelinolysis
acute tubular necrosis
fetal: small for gestational age, pre-term birth
Mx of hyperemsis gravidarum
antihistamines should be used first-line (BNF suggests promethazine as first-line)
ginger and P6 (wrist) acupressure: NICE Clinical Knowledge Summaries suggest these can be tried but there is little evidence of benefit
admission may be needed for IV hydration
Mx of primary herpes infection within 6w of delivery
Oral aciclovir 400 mg TDS (three times daily) until delivery is recommended in the RCOG guidelines for women who present with a primary herpes infection in their third trimester of pregnancy, especially if the woman is expected to deliver within 6 weeks.
When is IV aciclovir indicated in HSV infection during pregnancy?
IV aciclovir for the mother or for the infant is only recommended if there has been a preterm pre-labour rupture of membranes or a spontaneous vaginal delivery in the presence of a primary herpes infection.
What are the ToRCH infection?
toxoplasmosis, other, rubella, CMV, herpes
HSV 6w before delivery?
It can be difficult to differentiate between a primary infection and a recurrent infection and the guidelines recommend suppressive therapy for both infections after 36 weeks until delivery. Recommended method of delivery in a primary infection is a Caesarean section. For a recurrent infection the risk of transmission is low due to maternal antibodies and a Caesarean section is not recommended.
Mx of HSV
Management
gingivostomatitis: oral aciclovir, chlorhexidine mouthwash
cold sores: topical aciclovir although the evidence base for this is modest
genital herpes: oral aciclovir. Some patients with frequent exacerbations may benefit from longer term aciclovir
A 22-year-old woman presents with a thin, purulent, and mildly odorous vaginal discharge. She also complains of dysuria, intermenstrual bleeding and dyspareunia. A swab shows a Gram negative diplococcus.
IM ceftriaxone + oral azithromycin
The 2011 British Society for Sexual Health and HIV (BASHH) guidelines recommend ceftriaxone 500 mg intramuscularly as a single dose with azithromycin 1 g oral as a single dose. The azithromycin is thought to act synergistically with ceftriaxone and is also useful for eradicating any co-existent Chlamydia infections
A 27-year-old woman complains of an offensive ‘musty’, frothy, green vaginal discharge. On examination you an erythematous cervix with pinpoint areas of exudation.
The correct answer is Oral metronidazole
The ‘strawberry cervix’ is actually quite rare outside of examinations - some studies suggest only 2% of patients with Trichomonas vaginalis have this finding
A 30-year-old woman presents with an offensive ‘fishy’, thin, grey vaginal discharge. Testing the discharge shows the pH to be > 4.5.
Oral metronidazole
Amsell’s criteria for BV Dx?
Amsel’s criteria for diagnosis of bacterial vaginosis - 3 of the following 4 points should be present:
thin, white homogenous discharge
clue cells on microscopy: stippled vaginal epithelial cells
vaginal pH > 4.5
positive whiff test (addition of potassium hydroxide results in fishy odour)
Mx of PPH
ABC
IV syntocinon (oxytocin) 10 units or IV ergometrine 500 micrograms
IM carboprost
other options include: B-Lynch suture, ligation of the uterine arteries or internal iliac arteries
if severe, uncontrolled haemorrhage then a hysterectomy is sometimes performed as a life-saving procedure
Secondary PPH
occurs between 24 hours - 12 weeks**
due to retained placental tissue or endometritis
Primary PPH
occurs within 24 hours
affects around 5-7% of deliveries
most common cause of PPH is uterine atony (90% of cases). Other causes include genital trauma and clotting factors
Use of PGE2 in pregnancy?
Initiating labour
SFD
IUGR
Patau’s syndrome
(Trisomy 13)
Edwards syndrome
(Trisomy 18)
Exomphalos
Gastroschisis
Draw Mx of GDM
Risk assessment for VTE
High
Intermediate
Moderate
What are the risk factors for osteoporosis
Genetic
Constitutional
Environmental
Drugs
Disease
Statuatory grounds for abortion in the UK
Sites of ectopics
