General gynae Flashcards
Types of contraception
MEC
Cat 1 - no restrictions
Cat 2 - advantages outweigh theoretical or proven risks
Cat 3 - theoretical or proven risks outweigh advantages
Cat 4 - Unacceptable health risk
- age, obesity, medical co-morbs, preg status, cancer
Types of IUCD
All levonorgestrel based
Jaydess: 13.5mg LNG, 6ug daily, 3 years
Mirena: 52mg LNG, 20ug daily, 5-8 years
- stops release of egg from ovary
- inhibits sperm from reaching/ fertilising egg
- thins lining of the uterus
- thickens cervical mucus
IUCD insertion and removal in pregnancy
If HCG +ve, IUCD should be removed
IF PP, insert after 6/52 to minimise risk of expulsion
Insert immediately after 1st/ 2nd trimester loss
IUCD insertion in PID
If acute PID, do not insert
If already inserted, continue
Types of progesterone only contraceptives
POP - noretistherone 350ug (noriday), desogestral 5ug/day (cerazette)
- cerazette more likely to inibit ovulation
Implant- etonorgestral 68mg, 3 yrs
Depot - medroxyprogesterone acetate every 13/52
96-99% effective
Special considerations in using progesterone only contraceptives
<18/ >45 DMPA - slight reduction in BMD
Review on a 2 year basis
Progesterone may potentiate: CVD risk factors, HTN, obesity, DM
IHD/ stroke - MEC 3
GTD (neg/ pos/ unresponsive HCG)- MEC 1
Types of combined hormonal contraceptives
COCP
- first line
- low dose ethinyl estradiol < 35ug and progesterone
- incr. VTE risk
Other routes: patch, ring
99% effective
Special considerations in prescribing CHCs
> 40: MEC 2. Can be used up to 50 if no CI
PP: breastfeeding <6/52: MEC 4
- 6/52 - 6/12 MEC 2
- Not BF: can be given after 3/52 if no RF (MEC 2)
<24/40 loss: can be given immediately
Smoker:
- <35: MEC 2
- >35: MEC 3/4
- Ex-smoker > 1 yr: MEC 2
Obesity:
- BMI 30-34: MEC 2
- BMI >35: MEC 3
Avoid in HTN
Prev obs chole - not CI, MEC 2
FHx VTE <45yrs: MEC 3
Surgical precautions and CHCs
Major surgery:
- stop COCP 3/52 before, restart 2/52 postop
Minor:
- no need to stop
Types of emergency contraception
Copper coil: 1-120 hours UPI or within 5/7 of ovulation
Oral progesterone:
- ullipristal acetate (19 norprogesterone): within 120 hours UPI
- 1/5mg LNG 0-72 hours UPI
Best emergency contraceptive if breastfeeding > 6/52
Progesterone only pill
Best emergency contraceptive if trophoblastic disease
CuIUCD
Sterilisation procedure female
Lap or hysteroscopic
Failure rate 2-5/1000
Increased risk of ectopic pregnancy
Reversal possible w TL
Drugs that are enzyme inducers
Rifampicin
Phenytoin
COCP
Phenobarbitone
Carbamazepine
Spironolactone
Sterilisation procedure male
Done under LA
Failure risk 1/2000
Effectiveness natural methods contraception
Requires regular cycle
80-98% effective
Features of female condom/ diaphragm
Need spermicide
Requires fitting
Reusable
Remain in situ 6 hours post intercourse but < 30
Not protective against STIs
92-98% effective
What to do if one missed pill (COCP)
Take the last pill you missed, even if it means taking 2 on1 day
Still protected from pregnancy
What to do if >1pill missed (COCP)
- protection against pregnancy may be affected
Should: - take the last pill you missed when remembered
- leave any earlier missed pills
- Carry on with the rest of the pack as normal
- use extra contraception for 7/7
At end of pack: - if 7+ pills left, finish the pack and start 7 day pill-free break as normal
- if <7 pills left, finish the pack and start a new pack right away
What to do if POP missed
Take as soon as possible
- noriday 3 hours
- cerazette 12 ours
Additional contraception. for 2/7 is required
Emergency contraception if UPI in the 2/7 after pill missed
Recommended interpregnancy window
1 year
< 1 yr assoc w increased adverse obstetric outcomes
Points on lactation amenorrhoea method
Caveats:
- exclusive BF
- <6/12 pp
- fully amenorrhoeic
to be 98% effective
IUD insertion and PP period
PPIUC: first 48 hours after CS, from 10min after delivery of placenta
Expulsion 0-17%
Complications: uterine perf, infection
Follow up 4-6/52 post
Emergency contraception in PP period
UPI 21/7 after childbirth - is indicated
EllaOne doubled if BMI>35, or on enzyme inducers
Must stop breastfeeding for 1/52
Progesterone contraceptives in PP period
Safe
Depo and POP can be started immediately after childbirth
When can COCP be prescribed postpartum
Generally >6/52
- <3/52 and VTE risk factors = MEC4
- <3/52 and no VTE risk factors = MEC 3
- 3-6/52 and VTE risk factors = MEC 3
- 3-6/52 and no VTE risk factors = MEC 2
- > 6/52. = MEC 1
COCP preventative effects Ca
Ovarian CA
- risk reduction by 30-35%
- <6/12 use provides protection
Endometrial CA
- risk reduction by 50%
Colorectal CA
- risk reduction by 40% if used for >96 months
COCP non-contraeptive benefits - gynae disorders
Functional ovarian cysts
- prevent ovulation –> cyst reduction
Endometriosis
- reduction of menstrual blood flow
Fibroids:
- determined by estrogens. Anti-estrogenic affect of progestergens. protective against fibroids
Therapeutic non-contraceptive benefits of COCP
HMB
- reduces blood loss 50%
Dysmenorrhoea
- ovulation suppression
PMS
- Ovulation suppression
Endometriosis
- reduced menstrual flow
Acne:
- reduced steroid production
Diagnosing severe PMS
Prospective recording. of sx over 2 cycles w sx diary
Definitive dx w 3/13 GnRH analogues if sx diary not conclusive
Simple measures for managing PMS
COCP
Vit B6
SSRI
Management options for severe PMS
Integrated holistic approach
CBT if severe
Hormonal: drospirenone COC 1st line, lowest possible dose progesterone
Danazol - breast symptoms (irreversible. virilising effects)
GnRH analogues - w most severe symptoms only. LT use needs yearly dexa scan
Non-hormonal - SSRIs, spironolactone
Pre-pregnancy counselling (sx abate at pregnancy)
TAH + BSO - coonsider test of cure w GnRH first and ensure HRT tolerated
Treatment algorithm for PMS
First line:
- Exercise, CBT, Vit B6
- COCP
- Continuous or luteal (D15-D28) low dose SSRi
Second line:
- Estradiol patches + micronised progesterone D17-28/LNGIUS
- Higher dose SSRI continuously or luteal phahse
Third line:
GnRH. analogues and add-back HRT(continous combined estrogen + progesterone)
Fourth line:
- surgical rx +/- RHT
Prevalence of PCOS
10-15%
Symptoms of PCOS
Menstrual disturbance
Hyperandrogenism: acne, hihrsuitism, alopecia
Fertility problems
Obesity
Psychological
Longterm sequelae of PCOS
Type II DM
Dyslipidaemia
HTN
CVS disease
Endometrial Ca
Diagnosis of PCOS
Rotterdam criteria - must have 2 of 3
- oligomenorrhoea and/or anovulation
- clinical and/or biochem hyperandrogenism (low SHBG, free testosterone mildly elevated)
- PCO on USS: >/= 122 follicles measuring 2-9mm +/-increased ovarian volume
NB diagnoses to exclude before dx PCOS
Cushings
Androgen secreting tumour
Thyroid dysfx
CA
Hyperprolactinaemia
Serum endocrinology findings in PCOS
Inc or normal androgens (free testosterone and androstenedione)
Inc or normal LH (elevated in 40%, usually slim women)
Normal FSH
Inc or normal fasting insulin - not routinely measured; GTT done to screen for insulin resistance
Reduced or normal SHBG –> results in elevated “ free androgen index”
Inc or normal estradiol
Increased AMH
Pathophysiology of PCOS
Maybe genetic
Raised ovarian androgens –> multple follicles and PCO appearance
Increased LH –> increased androgen production
Decr SHBG - causing hihghh circulating freeandrogens
- levels inversely proportional to BMI
Insulin augments LH activity –> inc. resistance, incr LH activity –> inc ovarian androgens.
Investigations for PCOS
USS
Bloods: HCG, FSH, LH, PRL, am 17-hydroxyprogesterone, glucose, lipids, free testosterone, SHBG
* incr LH:FSH ratio
Rx for PCOS related hirsuitism
Dianette - ethinyloestradiol 35ug and cyproterone avetate 2mg (antiandrogen)
Estrogens –> incr SHHBG
- dianette can also help w acne
Managing PCOS related infertility
40-50% overweight
Ovulation at 6/12 - BMI <25 = 79%, BMI >35 = 12%
Clomiphene (antioestrogen) at D2-6 for ovulation induction
- 6/12 trial - monitor in first cycle w serial US and progesterone
Follicle tracking - conception rate 40%
Ovarian drilling: decr LH and inc SHBG - lower risks of multiple/ OHSS
- elevated FSH = good prognostic amrker
Managing PCOS related menstrual disturbances
Cyclical COCP/ medroxyprogesterone 10mg for 12/7 every 3/12 for at least 4 bleeds
- menstrual shedding NB to avoid hyperplasia
If not eager for cyclical hormones/ oligomenorrhoeic - US for ET every 6-12/12
- ET >10mm –> artificially induce bleed
- mirena for endometrial protection
Metformin 850mg bd - 8% conception rate. Used D2-6. Decreases circulating androgens and improves ovulation in those w BMI >25 and no response to clomid
Eg. benign ovarian mass
Functional cyst
Endometriomas
Serous cystadenoma
Mucinous cystadenoma
Mature teratome
Benign non-ovarian tubal masses
Paratubal cyst
Hydrosalpinges
Tubo-ovarian abscess
Peritoneal pseudocysts
Appendiceal abscess
Diverticular abscess
Pelvic kidney
Primary malignant ovarian mass
Germ cell tumour
Epithelial carcinoma
Sex-cord tumour
Secondary malignant ovarian masses
Predom breast of GI carcinoma
Bloods required in all women <40 w complex ovarian mass
LDH
AFP
HCG
Risk of Malignancy index
RMI = U x M x Ca 125
U - ultrasound features: multilocular cysts, solid areas, metastases, ascites, bilateral lesions
U = 0 (no signs)
U= 1 (1 sign)
U = 3 (2+ signs)
M - menopausal status
Pre= 1
Post = 3
* RMI> 200 = high risk
IOTA group ultrasound rules: B-rules vs M-rules
B-Rules : benign
- unilocular cyst
- presence of solid components where the largest solid component <7mm
- Presence of acoustic shadowing
- smooth multilocular tumour w largest diameter <100mm
- no blood flow
M-RUles: Malignant
- irregular solid tumour
- ascites
- at least 4 papillary structures
- irregular multilocular solid tumour with largest diameter >100mm
- very strong blood flow
Management of ovarian cyst
Simple cyst < 50mm - no follow up, will likely resolve spont
Simple cyst 50-70mm: yearly follow up
Simple cyst >70mm: further imaging/ surgery
Persisting cyst - surgery
Surgical approaces:
- lapasoscopic : benign
- laparotomy : large solid (eg dermoids)
- avoid rupture of spillage
- oophorectomy - discuss preop
- aspiration: less effective and assoc w high rates of recurrence
Causes of adnexal masses in pregnancy
Corpus luteal cyst
Follicular cyst
Haemorrhagic cyst
Hyper-stimualted ovaries
Hyperreactio luteinalis
Luteoma of pregnancy
Heterotopic pregnancy
Mature cystic teratome
Malignant germ cell tumour
PID
Appendiceal mass
Defn and risks with luteoma of pregnancy
Luteinised stroma cells replace the ovarian parenchyma
Incr androgen production
Androgens cause maternal virilisation in 25-30%
50% risk fetal virilisation
Features of corpus luteal cyst
CL provides progesterone support in T1
Spontaneously regress at 8/40
Highly vascular and prone to rupture or haemorrhage
Complications of hyperstimulated ovaries
OHSS
Ovaries >12cm
High risk torsion and haemorrhage
Usually self-limiting, requiring supportive rx
What is hyperreactio luteinalis
Exaggerated response to circulating levels of BHCG in thhe absence of ovulation –> grossly enlarged ovaries bilaterally; bilateral large theca lutein cysts
Assessment of ovarian mass in pregnancy
Imaging: USS, colour doppler, MRI/ CT
Tumour markers:
- Ca 125 - higher cut off in pregnancy, 112U/ml
- LDH - dysgerminoma
- AFP - limited in pregnancy, linked w germ cell tumours
- HE4 - glycoprotein expressed by epididymal epithelium; lower in pregnancy
RMI
Indications for surgery w ovarian mass in pregnancy
Acute abdomen
Mass suspicious for malignancy
Rapidly growing masses (inc in size > 20% = high risk for malignancy)
Cysts > 10cm which may obstruct labour
Incidence and features of adnexal torsion in pregnancy
1-5 per 10000 pregnancies
16% OSS
P/W acute abdo - CRP rise 6-8 hours, peaks at 24-72 hours
Management ovarian mass in pregnancy
MDT
Rescan 6/52 postnatal if no intervention
Conservative - 76% simple cyst, <5cm. Often resolve spont by 16/40. - follow up scan at 14-16/40 if larger/ complex
US guided FNA
Surgery
Advantages and disadvantages of laparoscopy in pregnancy
Adv: less blood loss, improved visualisation, less uterine irritability
Disadv: pneumoperitoneum - concern hypercarbia –> acid-base disturbances which reduce placental flow
Incidence of fibroids.
70-80% women
Risk factors for fibroids
Nulliparity
Early menarce
Increased nmenses frequency
Dysmenorrhoea
Family history
Obesity
Age
Clinical presentation fibroids
AUB
HMB
IDA
Pelvic pain/ pressure
Bowel/ bladder dysfunction
Fibroids and pregnancy
Stay same size or smaller
Concern re malpresentation or PTL
Incidence of malignant change in fibroids
Change to leiomyosarcoma - <1%
1 in 400
Pathogenesis fibroids
Monoclonal tumours arising from uterine smooth muscle
FIGO leiomyoma subclassification system
S- Submucosal
- 0: pedunculated intracavitary
- 1: <50% intramural
- 2: >/= 50% intramural
O - Other
- 3: contacts endometrium, 100% intramural
- 4: Intramural
- 5: Subserosal >/= 50% intramural
- 6: subserosal <50% intramural
- 7: subserosal pedunculated
- 8: other (e.g. cervical, parasitic)
Hybrid leiomyomas - impact both endometrium and serosa
Management algorithm uterine fibroids
Asymptomatic –> clinical surveillance
Symptomatic –> pre vs postmenopause
- Premenopause:
— enhance fertility: consider removal submucosal fibroids; no proven benefit to removing intramural and subserosal wrt fertility
— retain fertility (AUB): medical rx (ullipristal, OC, danazol, LNG-IUS, TXA, GnRH agonist). OR surgical (myomectomy)
— retain uterus (bulk effects +/- AUB): medical (ullipristal/ SPRM, GnRH agonist +/- add-back) OR surgical (myomectomy)
— other (bulk effects +/- AUB): interventional therapy (UAE, MRg-FUS, myolysis) OR surgical (myomectomy +/- EA)
- Postmenoapuse:
— TAH +/- BSO.
— hysteroscopic myomectomy
Causes of chronic pelvic pain
Can have several contributing factors
Endometriosis - pelvic, usually cyclical
Adhesions
IBS
MSK
Nerve entrapment
Psychological/ social
Ix for chronic pelvic pain
Screening for infection - PID
STI screen
TVUS to o/r masses
Dx lap
Mx chronic pelvic pain
Cyclical - offer COCP for 3-6/12 before dx lap
IBS - antispasmodics, diet
Analgesia
Clinical presentation endometriosis
Chronic pelvic pain
Cyclical pain
Dysmenorrhoea
Dyspareunia
HMB
Cyclical GI sx
Cyclical urinary sx
Infertility + symptomatic
Ix for endometriosis
Pain and symptom diary
Refer - severe, persistent, recurrent sx; pelvic signs
US: TV normal or presence of endometriomas
MRI: consider if ? extend to deep endo involving bladder and bowel
Dx lap : + biopsy
Management endometriosis
Analgesia - paracetamol, NSAIDS
Hormonal - COCP
Surgical
- consider 3/12 GnRH before surgery
- excision
Key points in managing endo when fertility is a priority
Offer excision or ablation + adhesiolysis if endo not involving bowel/ bladder/ ureter
Offer lap ovarian cystectomy if endometriomas
Do not offer hormonal contraception if TTC
Discuss benefits and risks of laparoscopy for deep endo:
- effect on future pregnancy
- possible impact on ovarian reserve
- the effect of complications on fertility
- Alternatives to surgery
- other fertility factors
Most common causes of PID
Chlamydia
Gonorrhoea
25% of cases
First line management of PID (mild)
Ceftriazone1g stat IV/IM
Doxycycline 100mg bd po x 14/7 (azithro if pregnant)
Metronidazole 400mg bd po x 14/7
Longterm sequelae of PID
Recurrence
Hydrosalpinx
Chronic pelvic pain
Infertility
Ectopic if tubal damage
Ovarian Ca
What to do if PID not improving on Abx
Consult micro
Check swabs
Pelvic USS
Consult other specialties if concerned
Laparoscopy - abscess drainage, washout, adhesiolysis
Fitz-Hugh-Curtis syndrome
RUQ pain and perihepatitis in PID
Symptoms of PID
B/L LAP
Dyspareunia
Abnormal PVB
Abnormal PV DC
Adnexal tenderness
CET
Pyrexial
PID management - severe
Ceftriazone 2g iV daily
Doxy 100mg bd x 14/7
Metro po/ IV
Should trace contacts
Preg test
GUM workup
Causes of superficial dyspareunia
Atrophy
Condylomatas
Infectious lesions
Trauma
Vulvodynia
Vulvovaginitis
Causes of deep dyspareunia
Adenomyosis
Endometriosis
Hig-tone pelvic floor dysfx
Interstitial cystitis
IBS
Pelvic adhesive disease
Pelvic congestionsyndrome
PID
Sexual abuse hx
Uterine leiomyomas
Uterine retroversion
Other generalized pain disorders
WHO classification of disorders of anovulation
Type 1: Hypogonadotrophic Hypogonadism:
- primary or secondary amenorroea, low levels endogenous gonadotropins and negligible endogenous estrogen activity
Type 2: Normogonadotrophic hypogonadism
- anovuation assoc w. a variety of menstrual disorders who exhibit distinct endogenous estrogen activity and gonadotrophin in the normal range
Type 3: Hypergonadotrophic hypogonadism
- primary or secondary amenorrhoea d/t primary ovarian failure assoc w low estrogen activity and pathologically high gonadotropin levels
Type 4: hyperprolactinaemia
Definitions in menstruation:
- normal cycle
- oligo
- poly
- menorrhagia
- metrorrhagia
- amenorrhoea
Normal: 21-35 days
Oligo: >35 days, <9/year
Poly: < 21 days
Menorrhagia: reg but excessive >80ml in 7/7
Metrorrhagia: irreg
Amenorrhoea: no menses
Causes of hypogonadotrophic hypogonadism
Congenital: Kallmann
Infiltrative: sarcoid, haemochromatosis
Drugs: glucocorticoids, narcotics
Infections: meningitis, encephalitis, TB
Head trauma or SOL: tumours and/or their rx
Causes of hypothalamic amenorrhohea
Excessive exercise
Eating disorders
Nutritional deficits
Psychological stress
Critical illness
Chronic illness (malabsorption syndromes)
Causes of hypopituitarism
Empty sella syndrome - aplasia/ hypoplasia or ant pituitary
Isolated pituitary hormone deficiency
Multiple pituitary hormone deficiencies
Syndromes assoc w pituitary ormone abnormalities
Trauma
Infection: meningitis, encephalitis, sarcoid, TB
Infiltration: langerhans cell histiocytosis, haemachromatosis, thal
Pituitary tumours and/or rx w surgery, chemo or radiation
Sheehan’s syndrome
Defn primary amenorrhoea
Absence of menses
- ix at 13/14 yo if no secondary sexual characteristics
- ix at 15/16yo if has secondary sexual characteristics
Incidence of primary amenorrhoea
3-4%
Pathophysiology primary amenorrhoea if +ve secondary sexual characteristics
High FSH:
- arrested puberty
- karyotype and. pelvic imaging
- DDx POF 46XX, CAIS (46XY, sort vagina, absent uterus)
Normal FSH:
- hypothalamic pituitary ovarian axis normal, amenorrhoea = anatomical defect
- Pelvic imaging: absent uterus (Mayer-Rokitanksy-Kuster-hauser syndrome), or obstructive anomaly - imperforate hymen, vaginal septum, vaginal/ cervical agenesis
Pathophysiology of primary amenorrhoea if no secondary sexual characteristics
Low FSH:
- central deficit
- constitutional
High FSH:
- peripheral - defect @ gonad
- Mat have prepubertal size uterus
- Turners. XO, Swyer 46XY, POF 46XX
NB social history when counselling amenorroeic patient
HEADSSS
- Home
- Education
- Activities
- Drinking/ drugs
- Sex
- Safety
- Suicide
Ix in primary amenorrhoea
BHCG
TSH, PRL
LH, FSH
+/- andogen screen
+/- estradiol
Definition of secondary amenorrhoea
Cessation of previously normal menstruation for >3 cycles or 3-6/12
Causes of secondary amenorrhoea - central
Hypothalamic
- low BMI: wt loss –> hypo hypo
- excessive exercise
- hyhpothalamix. lesions (craniopharyngiomas, gliomas, dermoid cysts –> compress hypothal/ block dopamine)
- systemic disease eg sarcoid/ TB
- Head injury/ cranial irradiation –> hypo hypo
Pituitary
- PRL-secreting adenoma: micro < 1cm, macro >1
- Sheehan syndrome
Causes of secondary amenorrhoea - GUT
Ovarian:
- PCOS
- POF - commonest=. AI ovarian antibodies
— Turners mosaic
— Infection
— Chemo/ rad
Genital tract abnormalities
- Ashermans
- Cx stenosis
Adrenal:
- virilising adrenal tumours
- late onset CAH
Causes of secondary amenorrhoea - systemic
Drugs:
- prev/ current use prog/ HRT
- dopamine antagonists
Systemic disease. eg Cushings
Chronic disease - liver/ renal/ thyroid
Investigations secondary amenorrhoea
BHCG
TSH, PRL, LH, FSH
+/- androgens. +/- estradiol
Progestin challenge- to test patient’s estrogen status
- course of progesterone x 7/7 –> if bleed, evidence that the patient is progesterone deficient, anovulatory or has an androgen excess
Estrogen/ progesterone challenge - course of E2/ P. If withdrawal bleeding = estrogen deficiency. If no bleeding, suspicious for anatomic abnormality
Likely diagnoses if bleeding wit progestin challenge
Gonadotrophic hypogonadism
- PCOS
- anovulation
- hypothhalamic/ pituitary dysfunction
- androgen excess
Differentials if + bleeding with estrogen/ progesterone challenge
Check FSH/ LH
FSH/ LH high = hypergonadotrophic hypogonadism
– menopause, POF
FSH/ LH low –> MRI
—MRI +ve for SOL
—MRI normal: hypogonadotrophic hypogonadism: low weight, anorexia, chronic illness
Causes of abnormal uterine bleeding
PALM COEIN
Polyp
Adenomyosis
Leiomyoma
Malighnancy/ hyperplasia
Coagulopathy
Ovulatory dysfx
Endometrial - primary disorder of mechanisms regulating haemostasis
Infection/ Iatrogenic (meds)
Not yet known
Significance of a fixed, retroverted uterus on exam
Inflammatory, adhesions
Red flags in AUB
>
- w new or worsening menorrhagia
Obese
Tamoxifen use or anastrozole use
Persistent, assoc intermenstrual or postcoital bleeding
PCOS
FHx endo Ca, Lynch
Failure of medical mx
Palpable mass
Anaemia not responding to rx
Management of AUB
Pharmacological:
- Non-hormonal
— PG synthase inhibitors- NSAIDS
— antifibrinolytics - TXA
- Hormonal:
— LNG IUS, COCP, norethisterone, Depo, GnRH
Surgical:
- endometrial ablation
- myomectomy
- UAE
- hysterectomy
Defn menopause
Final menstrual period followed by 12/12 amenorrhoea
Avg age 45-55 (avg age 51)
Defn PMB
episode of bleeding occurring 12+ months after final period
Causes PMB
Most often benign gynae conditions
- vaginal, endometrial atrophy d/t E2 deficiency
- endo. cervical polyps
- uterine prolapse
- endometritis
Incidence and RF endometrial Ca
in 90%. w PMB, only 9% endo Ca
12.4% PMB = endo hyperplasia
RF: tamoxifen, obesity, advanced age, HNPCC, unopposed E2
What to do w abnormal bleeding on HRT
Refer if persistent bleeding
Sequential HRT- irreg bleeding more than 3 months after commencing HRT or. increases in heaviness/ duration
Continuous HRT- bleeding beyond 6/12 of commencing or if bleeding commences after significant duration of amenorrhoea
What to do if incidental finding of ET >4mm and no PMB
If seen on CT/ MRI/ TAUS - TVUS to assess
If ET > 11mm –> sample
– risk of endo Ca is 6.7%
USS cut offs in PMB
Normal ET 3-5mm
No HRT 4mm
On HRT 5mm
TAUS if large uterus/ mass
When to use hysteroscopy for PMB
ET >4mm or focal endometrial pathology
Tamoxifen w abnormal bleeding (TVUS not useful)
Ambulatory or GA
Diagnosing menopause
Clinical - symptom history
Bloods: FSH >25 twice more than 2/52 apart
- 40-45 early
- <40 premature
Managing menopause
Nonhormonal
- clonidine - hoht flushes
Hormonal:
- HRT
- testosterone - lipido
CBT
- mood
Benefits of HRT
Eases menopausal symptoms
Improves vaginal dryness
Decreased risk of osteoporosis
Decrease risk CAD
Reduction in dementia
Risks assoc w HRT
VTE (not for patches/ gels)
Stroke - small incr risk w po E2
Breast Ca - related to duration of rx and returns to normal risk when rx. stopped
Risk of uterine ca stopped if combined used
Ovarian ca reduces to normal if stopped
Side effects HRT
Breast discomfort
Nausea
Irregular bleeding
Which HRT to use
Oestrogen alone - no uterus or mirena in situ
oestrogen + progesterone - uterus
Oestrogen preparations:
- patch
- tablet
- gel
- ring
Progesterone preparations
- LNGIUS
- pessaries
- tablets
Sequential HRT treatment plan
<1 year amenorrhoeic
Perimenopause
Uterus intact
Given oestrogen every day, progesterone 10-14 days
- reduces risk of endometrial ca
Combined HRT treatment plan
> 1 yr amen
3 yr on sequential
54yo
No uterus
- 10-14 d ays progesterone
- continuous E2
Symptom assessment (menopause) and rx
Dryness: topical E2, lubricants
Libido: testogel
Mood/ sleep: clonidine, SSRIs, tibilone
How to rx menopause w FHx breast Ca
Assess symptoms
Slight increase risk
- 4 extra in 1000 after 5 years
- same risk as. COCP
- increased risk w ETOH, smoking, BMI
- top E2 and mirena
Prevalence of hyperprolactinaemia
0.4-5%
Increases to 9% to women with amenorroea
25% if galactorroea
70% have hyperPRL if presenting wit amenorrohea and galactorrhoea
Physiology PRL
Stimulates epithelial cell proliferation
Induce milk production
Promotes formation and action of CL
Suppression of GnRH to decrease FSH/LH
DDx hyperprolactinaemia
Common:
- prolactinoma
- primary hypothyroidism
- drug-induced
- macroprolactinaemia
Uncommon:
- acromegaly
- hypothalamic mass compressing pituitary stalk
- MEN 1
Treatment hyperprolactinaemia
dopamie agonists
- reduce PRL and restore ovulation
- eg bromocriptine, cabergoline
Causes hyperprolactinaemia
Physiologic:
- pregnancy
- nursing
- nipple stimulation
- exercise
- stress
- sleep
- seizures
Pharmacologic:
- dopamine antagonist
- MOI
- cimetidine
- verapimil
- thyrotropin-releasing. hormone stimulation test
Pathologic:
- pituitary tumour
- hypothyroidism
- chronic renal insufficiency
- severe liver failure
- hypophysial stalk lesion
- neuraxis irradiation
- spinal cord lesions
- hypophysitis
- PCOS
Benefits of tibolone 2nd line over oestrogen
Bloating on oestrogen
Poor libido
Endometriosis
When to stop non-hormonal contraceptives in peri/post menopausal
40-50 yrs: stop after 2 years of amenorrhoea
>50 ys: stop after 1 year of amenorrhoea
When to stop COC in peri/post menopausal
40-50 yrs: can be continued
>50: stop at age 50 and switc to non-hormonal methohd or IMP/ POP/ LNG IUS/ then follow approp advice
When to stop progesterone only injectable in peri/ post menopausal
40-50 yrs: can be continued
>50: should be counselled regarding switchingto alternative metods
When to stop IMP/ POP/ LNG-IUS in peri/post menopausal
40-50 yrs: Can be continued to age 50 and beyond
>50: stop at age 55when natural loss of fertility can be assumed for most women
- if wants to stop before 55, check FSH level
- if FSH > 30iU/L - the IMP/ POP/ LNG-IUS can bediscontinued after 1 more year
- If FS level in premenopausal range, then method should be continued and FSH checked again in 1 year
