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Extra 5 (e) > Gynae 1 > Flashcards

Gynae 1 Flashcards

1
Q

What is premenstrual syndrome (PMS)?

A
  • Distressing psychological, physical and/or behavioural symptoms
  • Occurs during luteal phase with significant regression of symptoms with onset / during period
  • (if had hysterectomy with ovarian conservation = occurs cyclically)
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2
Q

How many people suffer from PMS?

A

15% asymptomatic
80% mild-moderate
5% severe

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3
Q

What is the aetiology of PMS?

A

Multiple

  • Cyclical ovarian likely to be the cause, thought that an ovarian trigger like ovulation can trigger a cascade of events
  • A central increased responsiveness to a combination of steroids, chemical messengers (such as E2, serotonin, progesterone, GABA) and psychological sensitivity may play a part
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4
Q

What are the signs/symptoms of severe PMS (DSM IV criteria)?

A

Equal to/>5 symptoms present for most of late luteal phase with remission within a few days onset of menses and absence of symptoms in the week post menses (must be at least 1 from first 4):

  • Markedly depressed mood, feelings of hopelessness or self-deprecation
  • Marked anxiety / tension
  • Marked affective lability (feeling suddenly sad or tearful)
  • Persistent and marked anger / irritability
  • Decreased interest in usual activities
  • Subjective sense of difficulty in concentrating
  • Lethargy
  • Marked change in appetite, overeating or specific food cravings
  • Hypersomnia or insomnia
  • Subjective sense of being overwhelmed or out of control.
  • Other physical symptoms (breast tenderness or swelling, headaches, joint or muscle pain, bloating, weight gain)
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5
Q

What investigations are done for PMS?

A

Mostly self-diagnosed

NB important to exclude organic disease or significant psychiatric illness

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6
Q

Ddx of PMS? (2)

A
  • Depression

- Neurosis

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7
Q

What are some hormonal managements of PMS?

A
  • Progesterone and progestrogens
  • Ovulation suppression agents:

COCP
Danazol
Oestrogen
GnRH analogues +/- addback HRT

NB addback HRT can alleviate undesirable hypo-oestrogenic effects such as bone demineralisation (ask ? )

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8
Q

What are some non-hormonal managements of PMS?

A
  • SSRIs / selective noradrenaline reuptake inhibitors
  • Antidepressants = tricyclics and anxiolytics
  • CBT
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9
Q

What are some self-help techniques for PMS?

A
  • Diet alterations ie less fat/sugar
  • Dietary supplements = Vit B6, Vit E, calcium, magnesium
  • Exercise
  • Stress reduction
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10
Q

What is PCOS?

A

Polycystic Ovary Syndrome

Polycystic ovary = a characteristic transvaginal US appearance of multiple (12 or more) small follicles (2-8mm) in an enlarged ovary (>10mL volume)

Women with PCO may develop other features of the full syndrome if they put on weight

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11
Q

What is the criteria used for diagnosing PCOS?

A

The Rotterdam criteria

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12
Q

What are the features of the Rotterdam criteria?

A

2 / 3 of:

1) Irregular or absent periods (>35 days apart)
2) Clinical/biochemical features of hyperandrogegism:
- Acne
- Hirsutism
- Alopecia
- Raised serum testosterone
3) Polycystic ovaries on USS

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13
Q

What is the pathogenesis of PCOS?

A

Not fully understood but likely to be multifactorial:

  • Excess androgens produced by theca cells of ovaries (either due to hyperinsulinaemia or increased LH levels)
  • Insulin resistance leading to hyperinsulinaemia in many women = weight gain further increases insulin resistance
  • Insulin resistance leads to:
    1) increased androgen production (multiple mechanisms)
    2) Reduced production of sex hormone-binding globulin (SHBG) in liver meaning free testosterone may be raised as testosterone binds SHBG (even if total testosterone normal)
  • Raised LH from anterior pituitary (in 40% women)
  • Raised oestrogen levels in some women can lead to to hyper plastic endometrium
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14
Q

How common is PCOS?

A

Most common endocrine disorder in women:

6-10% prevalence of women at childbearing age
Responsible for 80% of anovulatory subfertility

USS evidence of PCO in 20-30% women

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15
Q

What are some risk factors for PCOS? (2)

A
  • FH (familial clustering)
  • Obesity:
    1) BMI >30 is found in 35-60% of women with PCOS
    2) Central obesity
    = This worsens insulin resistance
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16
Q

What are some signs/symptoms of PCOS? (9)

A
  • May be asymptomatic
  • Signs of hyperaldosteronism = acne, hirsutism, alopecia
  • Obesity
  • Oligomenorrhoea (<9 periods per year) or amenorrhoea (due to chronic an ovulation)
  • Sub/infertility (75%)
  • Recurrent miscarriage (50-60%)
  • Ancanthosis nigricans (sign of insulin resistance)
  • Psychological symptoms eg mood swings
  • Occasionally signs of severe hyperandrogegism eg clitoromegaly, deep voice
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17
Q

What are some long term health consequences of PCOS? (4)

A
  • Obesity, insulin resistance and metabolic abnormalities (such as dyslipidaemia) are RF for IHD
  • DM2 is more common in women with PCOS
  • Increased risk of GDM
  • Long periods of secondary amenorrhoea is a RF for endometrial hyperplasia and carcinoma
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18
Q

What investigations are done for PCOS? (4)

A

1) Transvaginal / pelvuic USS

2) Bloods:
FSH 
- Raised in ovarian failure
- Low in hypothalamic disease
- Normal in PCOS

LH
- Often raised in PCOS but not diagnostic

TFTs

Prolactin
- To exclude a prolactinoma

Testosterone - if high:

  • Dehydroepiandrosterone sulphate (DHEAS)
  • Androstenedione
  • Sex hormone binding globulin (SHBG)

3) Screen for DM and abnormal lipids
4) BMI

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19
Q

List some ddx for PCOS (4)

A

1) Ovarian failure
2) Hypothalamic disease
3) Prolactinoma
4) Secondary cause of amenorrhoea

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20
Q

What is the management of PCOS? (6)

A

Lifestyle
- Weight loss / diet / exercise

Improve menstural regulatory:

  • Weight loss
  • COCP
  • Metformin

Control symptoms of hyperandrogegism:

  • Hair removal
  • Anti-androgens eg eflornithine face cream, finasteride, spironolactone = can be taken with acne/hirsiutism, takes 6-9 months to improve hair growth (NB avoid in pregnancy as feminises a male fetus)

Sub-fertility

  • Weight loss alone may achieve spontaneous ovulation
  • Ovulation induction with anti-oestrogens (clomifene) or gonadotrophin
  • Laparoscopic ovarian diathermy
  • IVF if ovulation cannot be achieved (risk of ovarian hyper stimulation)

Insulin sensitisers:
- Metformin = helps to regulate menstrual cycle and achieve ovulation (off licence for PCOS, no better than lifestyle modifications = doesn’t effect androgenic symptoms despite lowering androgen levels)

Psychological support

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21
Q

What is the average age of menopause?

A

52 years

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22
Q

What is menopause?

A

The permanent cessation of menstruation resulting in the loss of ovarian follicular activity

Natural menopause = 12 months of consecutive amenorrhoea for which no other pathological / physiological cause is present

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23
Q

What is perimenopause?

A

= Menopause transition. Begins several years before menopause, gradual time in which the ovaries make less oestrogen. There are clinical, biological and endocrinological features of approaching menopause eg vasomotor symptoms and menstrual irregularity, and ends with menopause (12 months after last menstrual period)

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24
Q

What is premenopause?

A

Either 1-2 years immediately before menopause or the whole of the reproductive period before menopause

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25
Q

What is postmenopause?

A

From final menstrual period (regardless of whether the menopause was induced or spontaneous)

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26
Q

What is climacteric?

A

The phase encompassing the transition from reproductive state to the non-reproductive state

ie menopause is a specific event occurring during the climacteric, just as menarche is an event that occurs during puberty

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27
Q

What is the physiology of menopause?

A

Cessation of the menstrual cycle due to ovarian failure leading to oestrogen deficiency

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28
Q

What are some short-term signs/symptoms of menopause? (3)

A

Vasomotor symptoms:

  • Hot flushes
  • Night sweats

Sexual dysfunction:

  • Changes in sexual behaviour and activity
  • Vaginal dryness (due to decreased oestrogen = can cause dyspareunia)
  • Low libido / problems with orgasm

Psychological symptoms:

  • Depressed mood
  • Anxiety
  • Irritability
  • Mood swings
  • Lethargy

Sleep disturbance

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29
Q

What are some long-term signs/symptoms of menopause? (4)

A
  • Osteoporisis = inc risk of fracture (esp Colles’, hip, vertebrae)
  • CV disease eg MI/stroke
  • Urogenital tract atrophy = freq, urgency, nocturne, incontinence, recurrent infection
  • Vaginal atrophy = dyspareunia, itching, burning, dryness
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30
Q

What investigations are done for menopause? (4)

A
  • FSH level only helpful if diagnosis is in doubt (eg <40yr) and levels in menopausal range (raised FSH is not diagnostic for menopause but a high level indicates a lack of ovarian response)
  • TFTs (T4 and TSH) to differentiate thyroid disease
  • Blood glucose as diabetes can cause similar symptoms
  • Check bone mineral density = significant RF for osteoporosis

UNHELPFUL TESTS = LH, estradiol, progesterone

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31
Q

What is the management of menopause?

A

Healthy lifestyle

HRT

  • Mainly helps with vasomotor symptoms, mood swings and vaginal/bladder symptoms
  • Usually improved within 4 weeks
  • Topical HRT can be useful for atrophic vaginitis
  • Prevents and reverses bone loss
  • Can help alleviate low mood (as can CBT - but no evidence that antidepressants help menopausal low mood)

Not many alternatives to HRT (eg if CI due to hormone-dependant tumours)

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32
Q

What is defined as premature menopause?

How common is it?

A

Menopause <40 year

20% of women

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33
Q

What are some causes of premature menopause?

A

Often no cause found

Primary causes:

  • Chromosome abnormalities
  • FSH receptor gene polymorphism and inhibit B mutation
  • Enzyme deficiencies
  • AI disease

Secondary causes:

  • Chemo / radiotherapy
  • Bilateral oophorectomy or surgical menopause
  • Hysterectomy without oopherectomy
  • Infection
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34
Q

What is are some signs/symptoms of premature menopause?

A

Most commonly amenorrhoea or oligomenorrhoea (+/- hot flushes)

Coexisting disease may be detected eg hypothyroidism, Addison’s disease, DM, chromosomal abnormalities

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35
Q

What are some consequences of premature menopause?

A
  • Inc risk of osteoporosis, CVD, breast cancer
  • Decreased peak bone mass (if <25yr) or early bone loss
  • Mean life expectancy is 2 years lower
36
Q

What is the management of premature menopause?

A

Oestrogen replacement needed until afterimage age of menopause - HRT, COCP

May have reduced fertility and require assisted conception

37
Q

What are the main indications for HRT? (3)

A

1) Treatment of menopausal symptoms where risk:benefit ratio is favourable
2) For women with early menopause until the age of natural menopause (51/52yr) even if they are asymptomatic
3) For women under 60 yrs who are at risk of an osteoporotic fracture in those where non-oestrogen treatments are unsuitable

Starting HRT is not recommended in those >60yr

38
Q

What combinations hormones are used in HRT?

A

Oestrogen alone = hysterectomy

Oestrogen + progestogen = non-hysterectomy

(progesterone does not need to be added if had hysterectomy = no protection required)

Others:
Tibolone (a synthetic steroid horomone) = converted to metabolites with oestrogenic, progestogenic and androgenic actions)

Testosterone (patches and implants) = improve libido

Micronised progesterone: ‘Body-identical progesterone’ = devoid of androgenic glucocorticoid activities but is slightly hypotensive (anti-mineralocorticoid acvity)

39
Q

What oestrogens are commonly used in HRT?

A

Estradiol
Estrone
Estriol
Conjugated quine oestrogen

40
Q

What progesterones are commonly used in HRT?

A

17-hydroxyprogesterone

  • Dydrogesterone
  • Medroxyprogesterone acetate

19-notestosterone derivatives

  • Norethisterone
  • Levonorgestrel
41
Q

What are some benefits of HRT? (7)

A

1) Reduction in vasomotor symptoms
2) QOL improvement eg sleep improvements
3) Improvement in mood changes
4) Improvement of urogenital symptoms
(systemic therapy does not improve urinary incontinence)
5) Reduction of osteoporosis risk
6) Reduction in CVD
7) Lower risk of colorectal cancer (by 1/3rd)

43
Q

What are some risks associated with HRT? (4)

A
  • Thromboembolic disease = VTE and PE (most likely in first year - note obesity greater RF)
  • Stroke
  • Breast and endometrial cancer = risk remained approx 5yrs after stopping HRT)
  • Gallbladder disease
44
Q

What are some delivery routes for HRT? (6)

A
  • Continuous or cyclical oral therapy
  • Patches
  • Creams or gels
  • Nasal sprays
  • Local devices such as progesterone-releasing IUS (levonorgestrel)
  • Oestrogen releasing vaginal ring
45
Q

When is transdermal vs Oral HRT preferred?

A

Transdermal oestrogen associated with fewer risks than oral HRT:

  • Advantageous for women with DM, prev VTE, thyroid disorders, history of migraine or gallbladder problems
  • Also less effect on clotting factors
  • Reduce triglycerides
46
Q

When is cyclical vs continuous HRT used?

A

Cyclical vs continuous

  • Cyclical if less than 1yr since LMP
  • Continuous if have used cyclical for >1yr OR >1yr since LMP OR at least 2 yrs since LMP if premature menopause
47
Q

What may happen initially to bleeding pattern with HRT?

A

Erratic bleeding can be commonin in first 3-6 months after starting HRT

If bleeding is heavy or irregular on cyclical HRT, dose of progestogen can be doubled / increased durating

Women with persistent vaginal bleeding >6mnths need further investigation

48
Q

What are some side effects of HRT? (oestrogen vs progesterone vs combined)

A

Oestrogen related:

  • Breast tenderness
  • Leg cramps
  • Bloating
  • Nausea
  • Headaches

Progesterone related:

  • Premenstural-like symptoms
  • Back ache
  • Depression
  • Pelvic pain

Combined HRT:
- Irregular, breakthrough bleeding

All types of HRT:
- Weight gain

49
Q

What investigations should be performed before starting HRT?

A

Not usually necessary unless:

  • Sudden change in menstrual pattern, IMB, PCB, postmenopausal bleeding = refer for endometrial assessment
  • Personal or family history of VTE = check with haematology
  • High risk of breast cancer = mammography / MRI
  • Arterial disease or risk factors = check lipid profile
50
Q

What is the first-line treatment for vaginal atrophy?

A

Topical oestrogen

However approx 10-25% women will still have symptoms so will require additional HRT

51
Q

List some ddx for chronic pelvic pain (8)

A

1) Endometriosis
2) Adhesions
3) IBS
4) Interstitial cystitis
5) MSK
6) Pelvic organ prolapse
7) Nerve entrapment
8) Psychological / social issues

52
Q

What is endometriosis?

A

The presence of endometrial like tissue outside of the uterine cavity

53
Q

What is it called if the ectopic endometrial tissue is within the myometrium itself?

A

Adenomyosis

54
Q

What hormone is involved in endometriosis thus who does it usually effect?

A

Oestrogen thus mostly affects women during their reproductive years

55
Q

List some common locations of endometriosis

A

Common = pelvis

  • Pouch of Douglas
  • Uterosacral ligaments
  • Ovarian fosse
  • Bladder
  • Peritoneum

Rare - lungs, brain, muscle, eye

56
Q

What is the incidence of endometriosis in:

  • General population
  • Infertility investigation
  • Sterilisation
  • Chronic pelvic pain investigation
  • Dysmenorrhoea
A 
General population = 10-12%
Infertility investigation = 20-30%
Sterilisation = 6%
Chronic pelvic pain investigation = 15%
Dysmenorrhoea = 40=60%

NB is the most common gynaecological condition after fibroids

57
Q

What is the aetiology of endometriosis? (4 theories)

A

Exact aetiology unknown, several theories

1) Retrograde menstruation with adhesion, invasion and growth of tissue:
- During menstruation, endometrium spills into the pelvic cavity through the Fallopian tubes (retrograde menstruation) and then implants and becomes functional, responding to hormones of the ovarian cycle

2) Metaplasia of mesothelial cells

3) Systematic and lymphatic spread:
- Endometrial tissues are transported by lymph or venous channels, explains rare cases of distant sites

4) Impaired immunity

58
Q

What are sone risk factors for endometriosis?

A

Almost exclusively in women of reproductive age (20-30s)

Factors that increase oestrogen exposure:

  • Early menarche
  • Late menopause
  • Delayed child bearing
  • Short menstrual cycles
  • Long duration of menstrual flow

Obstruction to vaginal outflow:

  • Hydrocolps
  • FGM
  • Defects in uterus / Fallopian tubes

Genetic:

  • Risk if first-degree relative has endometriosis = 6x greater
  • Familial clustering
  • ?Chr 7 and 10 links
59
Q

What are the 4 classic signs/symptoms of endometriosis? (4)

A

1) Secondary dysmenorrhoea
2) Deep dyspareunia
3) Pelvic Pain
4) Infertility

60
Q

Why does infertility arise in endometriosis?

A

Dense adhesions and resultant tubal / ovarian damage and distortion

Release of substances from ectopic endometrium (such as prostaglandins) can affect ovulation or affect tubal motility

61
Q

Why does pain arise in endometriosis (often chronic pelvic pain)?

A

Cyclic or constant pain = ectopic endometrial tissue undergoes the same menstrual cycle, causing repeated inflammation which may result in the formation of adhesions

62
Q

Why does dysmenorrhea arise in endometriosis?

A

Tends to occur prior to the beginning of the period and is exacerbated by the menstrual flow

63
Q

What may deep dyspareunia in endometriosis indicate?

A

Involvement of uterosacral ligaments

64
Q

What does dysuria in endometriosis indicate?

A

Involvement of bladder peritoneum or invasion on to the bladder

65
Q

What is dyschezia? What other rectal symptoms may arise in endometriosis?

A

Dyschezia = pain on defecation

May also get cyclic pararectal bleeding for rectovaginal nodules with invasion of rectal mucosa

66
Q

What other symptoms may occur in endometriosis? (3)

A
  • Chronic fatigue
  • Bleeding = heavier periods, or haematuria/rectal bleeding during menstruation
  • 2-50% asymptomatic

NB severity of symptoms tends to increase with age

67
Q

What are some complications of endometriosis? (6)

A 
Fibroids
Scarring
Infertility
Colonic/ureteric obstruction
Endometria rupture
Malignant change
IBD
68
Q

What may be found on examination in endometriosis? (5)

A
  • Adenexal masses = endometriosis ‘chocolate cysts’ or tenderness
  • Nodules/tenderness in posterior vaginal fornix or uterosacral ligaments
  • Thickening behind the uterus or adenexa
  • Fixed retroverted uterus
  • Rectovaginal nodules
69
Q

What investigations may be done for endometriosis?

A

Transvaginal USS:

  • Endometriomas
  • May find endometriosis in bladder or rectum

Laparoscopy with biopsy for histological verification (gold standard):

  • Note = symptoms and laparoscopic appearance do not always correlate
  • Whilst +ve is confirmative, -ve does not rule it out
  • Endometriomas >3cm should be resected to rule out malignancy (rare)
  • Should not be performed within 3 months of hormonal treatment (leads to under diagnosis)
  • Signs present = red dots, black ‘powder burn’ dots, large raised red/black vesicles, white area of scaring with surrounding abnormal blood vessels

MRI / IVU / barium enema:
- May be used to assess the extent of rectovaginal, bladder, ureteric or bowel involvement

Serum CA125 (sometimes raised in severe endometriosis)

70
Q

MOVE

What factors are protective for endometriosis? (2)

A

Multiparity

Oral contraceptives

71
Q

List some ddx for endometriosis (8)

A 
PID
Ectopic pregnancy
Torsion of an ovarian cyst
Appendicitis
Primary dysmenorrhoea 
IBS
Uterine fibroids
UTI
72
Q

What is an endometrioma?

A

A type of cyst formed when endometrial tissue grows in the ovaries

73
Q

What is the rASRM score for endometriosis? What 4 features does it include?

A

1) Location:
- Peritoneal
- Ovarian
- Pouch of Douglas

2) Size:
- <1cm
- 1-3cm
- >3cm

3) Depth
- Superficial
- Deep

4) Adhesions
- Filmy or dense
- Extent of enclosure

Stages minimal (I) to severe (IV)

74
Q

What is the medical management of endometriosis?

A

Pain management

COCP:
Effect = ovarian suppression

Medroxyprogesterone acetate or other progestagens
Effect = ovarian suppression
SE = weight gain, bloating, acne, irregular bleeding, depression

GnRH analoges (competitive occupancy of GnRH receptors)
Effect = ovarian suppression
SE = Loss of bone density (reversible), hot flushes, vaginal dryness, headaches, depression

Levonorgesterol releasingg IUS
Effect = endometrial suppression (sometimes ovarian)
SE = irregular bleeding, spontaneous expulsion

Danazol (anti-androgenic)
Effect = ovarian suppression
SE = irreversible voice changes, hirsutism, acne

Aromatase inhibitors
Effect = local oestrogen suppression in endometrial lesions
SE = ovarian cyst, loss of bone density (reversible)

All drugs are equally effective at pain management and associated with up to 50% recurrence after stopping

75
Q

What is the surgical management of endometriosis?

A

Coagulation, excision or ablation performed laparoscopically

Last resort = hysterectomy with sapling-oopherectomy

76
Q

What is the treatment of sub fertility in endometriosis?

A

Mild/moderatre - spontaneous pregnancy rate may increase after surgical removal of endometriosis lesions

Endometriomas >3m should be removed

IVF may be treatment of choice in moderate/severe cases

77
Q

What is pelvic inflammatory disease (PID)?

A

General term for infection of the upper female genital tract including the uterus (endometritis), Fallopian tubes (salpingitis), ovaries (oophoritis) or adjacent peritoneum (peritonitis)

Most commonly caused by ascending infection from the endocervix but may also occur from descending infections from organs such as the appendix

Severity ranges from chronic low grade (relatively mild symptoms) to acute infection (with severe symptoms) which may result in abscess formation

78
Q

Why is there a low threshold for empirical therapy of PID?

A

Increases risk of ectopic pregnancy and infertility

79
Q

Who is most at risk of PID?

A

Sexually active women aged 15-30

80
Q

What is the aetiology of PID?

A

90% sexually transmitted
10% follow pregnancy termination or dilatation ad curettage

Most common = chalmydia trachomatis. Also Nesseria gonorrhoea
- Also can be cased by endogenous organisms eg Mycoplasma hominis, Ureaplasma urealyticum

81
Q

What are some risk factors for PID? (6)

A

1) Age <25
2) Prev STI
3) New sexual partner / multiple partners
4) Uterine instrumentation eg IUD/ IUS
5) Postpartum endometritis
6) TOP

82
Q

What are some protective factors for PID? (2)

A

1) Barrer contraception

2) COCP - causes thickening of the cervical mucus which events the bacteria ascending

83
Q

What are some signs/symptoms of PID?

A

Can be asymptomatic (diagnosis only made retrospectively during investigation of sub fertility)

  • Bilateral lower abdo tenderness
  • Purulent vaginal discharge
  • Deep dyspareunia
  • Cervical motion tenderness
  • Adnexal tenderness

Severe:

  • Malaise
  • Nausea
  • Menstrual disturbance
  • Fever
  • Guarding
84
Q

What are some complications of PID? (5)

A
  • Tubo-Ovarian abscess/pyosalpinx
  • Fitz-Hugh-Curtis syndrome (perihepatitis = think in women <30yr presenting with RUQ pain)
  • Recurrent PID
  • Ectopic pregnancy
  • Infertility
85
Q

What investigations are done for PID?

A

Blood:

  • FBC
  • ESR / CRP
Swabs:
- High vaginal
- Endocervical
- Vulvovaginal
NB -ve does not exclude PID
Urinalysis
USS if tuba-ovarian abscess suspected
Laparoscopy = gold standard but only performed if tube-ovarian abscess suspected (invasive)
Pregnancy test (exclude ectopic)
86
Q

List some ddx for PID (8)

A 
Adnexal tumours
Appendictis
Ectopic pregnancy 
Endometriosis
Interstitial cystitis
Ovarian cysts
Ovarian torsion
87
Q

What is the management of PID?

A

Pain relief
Antibiotics (cover all organisms)

IM ceftriaxone 250mg + oral doxycycline 100mg BD + metronidazole 400mg BD for 14 days

OR

Oral ofloxacin 400mg BD + oral metronidazole 400mg BD for 14 days

Review after 72hrs to ensure adequate response to treatment

Inpatient care required if severe / failure to respond to treatment / a tubo-ovarian cyst is suspected

Contact tracing of partners essential and intercourse should be avoided during treatment

Drain tuba-ovarian abscess if present (US guided aspiration or laparoscopy)

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