General gynae Flashcards

1
Q

Types of contraception

A

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

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2
Q

Types of IUCD

A

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

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3
Q

IUCD insertion and removal in pregnancy

A

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

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4
Q

IUCD insertion in PID

A

If acute PID, do not insert
If already inserted, continue

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5
Q

Types of progesterone only contraceptives

A

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

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6
Q

Special considerations in using progesterone only contraceptives

A

<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

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7
Q

Types of combined hormonal contraceptives

A

COCP
- first line
- low dose ethinyl estradiol < 35ug and progesterone
- incr. VTE risk
Other routes: patch, ring
99% effective

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8
Q

Special considerations in prescribing CHCs

A

> 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

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9
Q

Surgical precautions and CHCs

A

Major surgery:
- stop COCP 3/52 before, restart 2/52 postop
Minor:
- no need to stop

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10
Q

Types of emergency contraception

A

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

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11
Q

Best emergency contraceptive if breastfeeding > 6/52

A

Progesterone only pill

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12
Q

Best emergency contraceptive if trophoblastic disease

A

CuIUCD

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13
Q

Sterilisation procedure female

A

Lap or hysteroscopic
Failure rate 2-5/1000
Increased risk of ectopic pregnancy
Reversal possible w TL

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13
Q

Drugs that are enzyme inducers

A

Rifampicin
Phenytoin
COCP
Phenobarbitone
Carbamazepine
Spironolactone

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14
Q

Sterilisation procedure male

A

Done under LA
Failure risk 1/2000

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15
Q

Effectiveness natural methods contraception

A

Requires regular cycle
80-98% effective

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16
Q

Features of female condom/ diaphragm

A

Need spermicide
Requires fitting
Reusable
Remain in situ 6 hours post intercourse but < 30
Not protective against STIs
92-98% effective

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17
Q

What to do if one missed pill (COCP)

A

Take the last pill you missed, even if it means taking 2 on1 day
Still protected from pregnancy

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18
Q

What to do if >1pill missed (COCP)

A
  • 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
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19
Q

What to do if POP missed

A

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

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20
Q

Recommended interpregnancy window

A

1 year
< 1 yr assoc w increased adverse obstetric outcomes

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21
Q

Points on lactation amenorrhoea method

A

Caveats:
- exclusive BF
- <6/12 pp
- fully amenorrhoeic
to be 98% effective

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22
Q

IUD insertion and PP period

A

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

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23
Q

Emergency contraception in PP period

A

UPI 21/7 after childbirth - is indicated
EllaOne doubled if BMI>35, or on enzyme inducers
Must stop breastfeeding for 1/52

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24
Q

Progesterone contraceptives in PP period

A

Safe
Depo and POP can be started immediately after childbirth

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25
Q

When can COCP be prescribed postpartum

A

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

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26
Q

COCP preventative effects Ca

A

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

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27
Q

COCP non-contraeptive benefits - gynae disorders

A

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

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28
Q

Therapeutic non-contraceptive benefits of COCP

A

HMB
- reduces blood loss 50%
Dysmenorrhoea
- ovulation suppression
PMS
- Ovulation suppression
Endometriosis
- reduced menstrual flow
Acne:
- reduced steroid production

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29
Q

Diagnosing severe PMS

A

Prospective recording. of sx over 2 cycles w sx diary
Definitive dx w 3/13 GnRH analogues if sx diary not conclusive

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30
Q

Simple measures for managing PMS

A

COCP
Vit B6
SSRI

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31
Q

Management options for severe PMS

A

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

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32
Q

Treatment algorithm for PMS

A

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

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33
Q

Prevalence of PCOS

A

10-15%

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34
Q

Symptoms of PCOS

A

Menstrual disturbance
Hyperandrogenism: acne, hihrsuitism, alopecia
Fertility problems
Obesity
Psychological

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35
Q

Longterm sequelae of PCOS

A

Type II DM
Dyslipidaemia
HTN
CVS disease
Endometrial Ca

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36
Q

Diagnosis of PCOS

A

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

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37
Q

NB diagnoses to exclude before dx PCOS

A

Cushings
Androgen secreting tumour
Thyroid dysfx
CA
Hyperprolactinaemia

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38
Q

Serum endocrinology findings in PCOS

A

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

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39
Q

Pathophysiology of PCOS

A

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.

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40
Q

Investigations for PCOS

A

USS
Bloods: HCG, FSH, LH, PRL, am 17-hydroxyprogesterone, glucose, lipids, free testosterone, SHBG
* incr LH:FSH ratio

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41
Q

Rx for PCOS related hirsuitism

A

Dianette - ethinyloestradiol 35ug and cyproterone avetate 2mg (antiandrogen)
Estrogens –> incr SHHBG
- dianette can also help w acne

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42
Q

Managing PCOS related infertility

A

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

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43
Q

Managing PCOS related menstrual disturbances

A

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

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44
Q

Eg. benign ovarian mass

A

Functional cyst
Endometriomas
Serous cystadenoma
Mucinous cystadenoma
Mature teratome

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45
Q

Benign non-ovarian tubal masses

A

Paratubal cyst
Hydrosalpinges
Tubo-ovarian abscess
Peritoneal pseudocysts
Appendiceal abscess
Diverticular abscess
Pelvic kidney

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46
Q

Primary malignant ovarian mass

A

Germ cell tumour
Epithelial carcinoma
Sex-cord tumour

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47
Q

Secondary malignant ovarian masses

A

Predom breast of GI carcinoma

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48
Q

Bloods required in all women <40 w complex ovarian mass

A

LDH
AFP
HCG

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49
Q

Risk of Malignancy index

A

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

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50
Q

IOTA group ultrasound rules: B-rules vs M-rules

A

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

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51
Q

Management of ovarian cyst

A

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

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52
Q

Causes of adnexal masses in pregnancy

A

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

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53
Q

Defn and risks with luteoma of pregnancy

A

Luteinised stroma cells replace the ovarian parenchyma
Incr androgen production
Androgens cause maternal virilisation in 25-30%
50% risk fetal virilisation

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54
Q

Features of corpus luteal cyst

A

CL provides progesterone support in T1
Spontaneously regress at 8/40
Highly vascular and prone to rupture or haemorrhage

55
Q

Complications of hyperstimulated ovaries

A

OHSS
Ovaries >12cm
High risk torsion and haemorrhage
Usually self-limiting, requiring supportive rx

56
Q

What is hyperreactio luteinalis

A

Exaggerated response to circulating levels of BHCG in thhe absence of ovulation –> grossly enlarged ovaries bilaterally; bilateral large theca lutein cysts

57
Q

Assessment of ovarian mass in pregnancy

A

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

58
Q

Indications for surgery w ovarian mass in pregnancy

A

Acute abdomen
Mass suspicious for malignancy
Rapidly growing masses (inc in size > 20% = high risk for malignancy)
Cysts > 10cm which may obstruct labour

59
Q

Incidence and features of adnexal torsion in pregnancy

A

1-5 per 10000 pregnancies
16% OSS
P/W acute abdo - CRP rise 6-8 hours, peaks at 24-72 hours

60
Q

Management ovarian mass in pregnancy

A

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

61
Q

Advantages and disadvantages of laparoscopy in pregnancy

A

Adv: less blood loss, improved visualisation, less uterine irritability
Disadv: pneumoperitoneum - concern hypercarbia –> acid-base disturbances which reduce placental flow

62
Q

Incidence of fibroids.

A

70-80% women

63
Q

Risk factors for fibroids

A

Nulliparity
Early menarce
Increased nmenses frequency
Dysmenorrhoea
Family history
Obesity
Age

64
Q

Clinical presentation fibroids

A

AUB
HMB
IDA
Pelvic pain/ pressure
Bowel/ bladder dysfunction

65
Q

Fibroids and pregnancy

A

Stay same size or smaller
Concern re malpresentation or PTL

66
Q

Incidence of malignant change in fibroids

A

Change to leiomyosarcoma - <1%
1 in 400

67
Q

Pathogenesis fibroids

A

Monoclonal tumours arising from uterine smooth muscle

68
Q

FIGO leiomyoma subclassification system

A

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

69
Q

Management algorithm uterine fibroids

A

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

70
Q

Causes of chronic pelvic pain

A

Can have several contributing factors
Endometriosis - pelvic, usually cyclical
Adhesions
IBS
MSK
Nerve entrapment
Psychological/ social

71
Q

Ix for chronic pelvic pain

A

Screening for infection - PID
STI screen
TVUS to o/r masses
Dx lap

72
Q

Mx chronic pelvic pain

A

Cyclical - offer COCP for 3-6/12 before dx lap
IBS - antispasmodics, diet
Analgesia

73
Q

Clinical presentation endometriosis

A

Chronic pelvic pain
Cyclical pain
Dysmenorrhoea
Dyspareunia
HMB
Cyclical GI sx
Cyclical urinary sx
Infertility + symptomatic

74
Q

Ix for endometriosis

A

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

75
Q

Management endometriosis

A

Analgesia - paracetamol, NSAIDS
Hormonal - COCP
Surgical
- consider 3/12 GnRH before surgery
- excision

76
Q

Key points in managing endo when fertility is a priority

A

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

77
Q

Most common causes of PID

A

Chlamydia
Gonorrhoea
25% of cases

78
Q

First line management of PID (mild)

A

Ceftriazone1g stat IV/IM
Doxycycline 100mg bd po x 14/7 (azithro if pregnant)
Metronidazole 400mg bd po x 14/7

79
Q

Longterm sequelae of PID

A

Recurrence
Hydrosalpinx
Chronic pelvic pain
Infertility
Ectopic if tubal damage
Ovarian Ca

80
Q

What to do if PID not improving on Abx

A

Consult micro
Check swabs
Pelvic USS
Consult other specialties if concerned
Laparoscopy - abscess drainage, washout, adhesiolysis

81
Q

Fitz-Hugh-Curtis syndrome

A

RUQ pain and perihepatitis in PID

82
Q

Symptoms of PID

A

B/L LAP
Dyspareunia
Abnormal PVB
Abnormal PV DC
Adnexal tenderness
CET
Pyrexial

83
Q

PID management - severe

A

Ceftriazone 2g iV daily
Doxy 100mg bd x 14/7
Metro po/ IV
Should trace contacts
Preg test
GUM workup

84
Q

Causes of superficial dyspareunia

A

Atrophy
Condylomatas
Infectious lesions
Trauma
Vulvodynia
Vulvovaginitis

85
Q

Causes of deep dyspareunia

A

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

86
Q

WHO classification of disorders of anovulation

A

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

87
Q

Definitions in menstruation:
- normal cycle
- oligo
- poly
- menorrhagia
- metrorrhagia
- amenorrhoea

A

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

88
Q

Causes of hypogonadotrophic hypogonadism

A

Congenital: Kallmann
Infiltrative: sarcoid, haemochromatosis
Drugs: glucocorticoids, narcotics
Infections: meningitis, encephalitis, TB
Head trauma or SOL: tumours and/or their rx

89
Q

Causes of hypothalamic amenorrhohea

A

Excessive exercise
Eating disorders
Nutritional deficits
Psychological stress
Critical illness
Chronic illness (malabsorption syndromes)

90
Q

Causes of hypopituitarism

A

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

91
Q

Defn primary amenorrhoea

A

Absence of menses
- ix at 13/14 yo if no secondary sexual characteristics
- ix at 15/16yo if has secondary sexual characteristics

92
Q

Incidence of primary amenorrhoea

A

3-4%

93
Q

Pathophysiology primary amenorrhoea if +ve secondary sexual characteristics

A

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

94
Q

Pathophysiology of primary amenorrhoea if no secondary sexual characteristics

A

Low FSH:
- central deficit
- constitutional
High FSH:
- peripheral - defect @ gonad
- Mat have prepubertal size uterus
- Turners. XO, Swyer 46XY, POF 46XX

95
Q

NB social history when counselling amenorroeic patient

A

HEADSSS
- Home
- Education
- Activities
- Drinking/ drugs
- Sex
- Safety
- Suicide

96
Q

Ix in primary amenorrhoea

A

BHCG
TSH, PRL
LH, FSH
+/- andogen screen
+/- estradiol

97
Q

Definition of secondary amenorrhoea

A

Cessation of previously normal menstruation for >3 cycles or 3-6/12

98
Q

Causes of secondary amenorrhoea - central

A

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

99
Q

Causes of secondary amenorrhoea - GUT

A

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

100
Q

Causes of secondary amenorrhoea - systemic

A

Drugs:
- prev/ current use prog/ HRT
- dopamine antagonists
Systemic disease. eg Cushings
Chronic disease - liver/ renal/ thyroid

101
Q

Investigations secondary amenorrhoea

A

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

102
Q

Likely diagnoses if bleeding wit progestin challenge

A

Gonadotrophic hypogonadism
- PCOS
- anovulation
- hypothhalamic/ pituitary dysfunction
- androgen excess

103
Q

Differentials if + bleeding with estrogen/ progesterone challenge

A

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

104
Q

Causes of abnormal uterine bleeding

A

PALM COEIN
Polyp
Adenomyosis
Leiomyoma
Malighnancy/ hyperplasia

Coagulopathy
Ovulatory dysfx
Endometrial - primary disorder of mechanisms regulating haemostasis
Infection/ Iatrogenic (meds)
Not yet known

105
Q

Significance of a fixed, retroverted uterus on exam

A

Inflammatory, adhesions

106
Q

Red flags in AUB

A

>

  1. 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
107
Q

Management of AUB

A

Pharmacological:
- Non-hormonal
— PG synthase inhibitors- NSAIDS
— antifibrinolytics - TXA
- Hormonal:
— LNG IUS, COCP, norethisterone, Depo, GnRH

Surgical:
- endometrial ablation
- myomectomy
- UAE
- hysterectomy

108
Q

Defn menopause

A

Final menstrual period followed by 12/12 amenorrhoea

Avg age 45-55 (avg age 51)

109
Q

Defn PMB

A

episode of bleeding occurring 12+ months after final period

110
Q

Causes PMB

A

Most often benign gynae conditions
- vaginal, endometrial atrophy d/t E2 deficiency
- endo. cervical polyps
- uterine prolapse
- endometritis

111
Q

Incidence and RF endometrial Ca

A

in 90%. w PMB, only 9% endo Ca
12.4% PMB = endo hyperplasia
RF: tamoxifen, obesity, advanced age, HNPCC, unopposed E2

112
Q

What to do w abnormal bleeding on HRT

A

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

113
Q

What to do if incidental finding of ET >4mm and no PMB

A

If seen on CT/ MRI/ TAUS - TVUS to assess
If ET > 11mm –> sample
– risk of endo Ca is 6.7%

114
Q

USS cut offs in PMB

A

Normal ET 3-5mm
No HRT 4mm
On HRT 5mm
TAUS if large uterus/ mass

115
Q

When to use hysteroscopy for PMB

A

ET >4mm or focal endometrial pathology
Tamoxifen w abnormal bleeding (TVUS not useful)
Ambulatory or GA

116
Q

Diagnosing menopause

A

Clinical - symptom history
Bloods: FSH >25 twice more than 2/52 apart
- 40-45 early
- <40 premature

117
Q

Managing menopause

A

Nonhormonal
- clonidine - hoht flushes
Hormonal:
- HRT
- testosterone - lipido
CBT
- mood

118
Q

Benefits of HRT

A

Eases menopausal symptoms
Improves vaginal dryness
Decreased risk of osteoporosis
Decrease risk CAD
Reduction in dementia

119
Q

Risks assoc w HRT

A

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

120
Q

Side effects HRT

A

Breast discomfort
Nausea
Irregular bleeding

121
Q

Which HRT to use

A

Oestrogen alone - no uterus or mirena in situ
oestrogen + progesterone - uterus
Oestrogen preparations:
- patch
- tablet
- gel
- ring
Progesterone preparations
- LNGIUS
- pessaries
- tablets

122
Q

Sequential HRT treatment plan

A

<1 year amenorrhoeic
Perimenopause
Uterus intact
Given oestrogen every day, progesterone 10-14 days
- reduces risk of endometrial ca

123
Q

Combined HRT treatment plan

A

> 1 yr amen
3 yr on sequential
54yo
No uterus

  • 10-14 d ays progesterone
  • continuous E2
124
Q

Symptom assessment (menopause) and rx

A

Dryness: topical E2, lubricants
Libido: testogel
Mood/ sleep: clonidine, SSRIs, tibilone

125
Q

How to rx menopause w FHx breast Ca

A

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

126
Q

Prevalence of hyperprolactinaemia

A

0.4-5%
Increases to 9% to women with amenorroea
25% if galactorroea
70% have hyperPRL if presenting wit amenorrohea and galactorrhoea

127
Q

Physiology PRL

A

Stimulates epithelial cell proliferation
Induce milk production
Promotes formation and action of CL
Suppression of GnRH to decrease FSH/LH

128
Q

DDx hyperprolactinaemia

A

Common:
- prolactinoma
- primary hypothyroidism
- drug-induced
- macroprolactinaemia

Uncommon:
- acromegaly
- hypothalamic mass compressing pituitary stalk
- MEN 1

129
Q

Treatment hyperprolactinaemia

A

dopamie agonists
- reduce PRL and restore ovulation
- eg bromocriptine, cabergoline

130
Q

Causes hyperprolactinaemia

A

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

131
Q

Benefits of tibolone 2nd line over oestrogen

A

Bloating on oestrogen
Poor libido
Endometriosis

132
Q

When to stop non-hormonal contraceptives in peri/post menopausal

A

40-50 yrs: stop after 2 years of amenorrhoea
>50 ys: stop after 1 year of amenorrhoea

133
Q

When to stop COC in peri/post menopausal

A

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

134
Q

When to stop progesterone only injectable in peri/ post menopausal

A

40-50 yrs: can be continued
>50: should be counselled regarding switchingto alternative metods

135
Q

When to stop IMP/ POP/ LNG-IUS in peri/post menopausal

A

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

136
Q
A