Gynae 1 Flashcards

1
Q

What is premenstrual syndrome (PMS)?

A
  • Distressing psychological, physical and/or behavioural symptoms in the absence of organic/psychiatric disease
  • Occurs during luteal phase with significant improvement 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 are the signs/symptoms of severe PMS (DSM IV criteria)?

A

5+ symptoms present for most of late luteal phase
Remission within a few days from onset of menses
Absence of symptoms in the week post menses (must be at least 1 from first 4):

  • Depressed mood, feelings of hopelessness or self-deprecation
  • Anxiety / tension
  • Affective lability (feeling suddenly sad or tearful)
  • Anger / irritability
  • Decreased interest in usual activities
  • Subjective sense of difficulty in concentrating
  • Lethargy
  • 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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4
Q

What investigations are done for PMS?

A

Mostly self-diagnosed - symptom diary filled in over 2 cycles

NB important to exclude organic disease or significant psychiatric illness

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5
Q

What are some hormonal management options of PMS?

A

Progesterone and progestrogens

  • Mirena coil
  • Depot injection

Ovulation suppression agents:

  • COCP
  • Danazol
  • Oestrogen
  • GnRH analogues +/- addback HRT

NB addback HRT reduces risk of bone demineralisation

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6
Q

What are some non-hormonal managements of PMS?

A
  • SSRI/SNRI - can take continuously or just during luteal phase
  • Total hysterectomy
  • CBT
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7
Q

What are some self-help techniques for PMS?

A
  • Diet alterations i.e. less fat, sugar, salt, caffeine
  • Dietary supplements - Vit B6 10mg OD
  • Exercise
  • Stress reduction
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8
Q

What defines a polycystic ovary?

A

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

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9
Q

What is the criteria used for diagnosing PCOS called?

A

The Rotterdam criteria 2003

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10
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 TVUS

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11
Q

What is the pathophysiology 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)

Raised LH from anterior pituitary (in 40% women)

Insulin resistance (often caused by weight gain) leads to hyperinsulinaemia

Insulin resistance leads to:

  • Increased androgen production (multiple mechanisms)
  • Reduced production of sex hormone-binding globulin (SHBG) in liver leading to raised levels of free testosterone
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12
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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13
Q

What are some risk factors for PCOS? (2)

A

Family history - genetic

Metabolic syndrome

  • Obesity (particularly central obesity)
  • Insulin resistance
  • Hypercholesterolaemia
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14
Q

What are some signs/symptoms of PCOS?

A

· Oligomenorrhoea (can be amenorrhoea too)
· Hirsutism – excessive male pattern hair growth
· Acne vulgaris
· Androgenic alopecia
· Infertility – due to chronic anovulation
· Obesity/signs of metabolic syndrome
· Acanthosis nigricans
· Voice change may occur in severe forms of PCOS but it typically suggests a different underlying cause of hyperandrogenism

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15
Q

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

A

· Gestational diabetes – should screen in pregnancy at 24-48 weeks
· Type 2 diabetes
· Cardiovascular disease
· Endometrial cancer – aim for 3-4 monthly withdrawal bleeds to reduce risk

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16
Q

What blood hormone levels are investigated in PCOS?

A

· Increased testosterone – both total and free

· Increase LH (LH:FSH ratio > 2:1) - a reversed LH:FSH ratio of around 3:1 is characteristic

· Oestrogen - normal/slightly elevated

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17
Q

List some ddx for PCOS

A

1) Ovarian failure
2) Hypothalamic disease
3) Prolactinoma
4) Secondary cause of amenorrhoea
5) Congenital adrenal hyperplasia

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18
Q

What are the 4 broad categories of medical management of PCOS?

A
  1. Lowering insulin levels
  2. Restoring fertility
  3. Treatment of hirsutism and acne
  4. Restoration of regular menstruation with prevention of endometrial hyperplasia and cancer
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19
Q

What is the average age of menopause?

A

52 years

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20
Q

What is menopause?

A

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

Natural menopause = 12 months of amenorrhoea in women > 50 or 24 months after LMP in women < 50

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21
Q

What is perimenopause?

A

= Menopause transition

The time period from the first instance of climacteric symptoms to multiple years post-menopause (average length = 4 years)

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22
Q

What is premenopause?

A

Time period from first occurrence of climacteric irregular menstruation cycles to the last menstrual period; characterised by increasingly infrequent menstruation

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23
Q

What is postmenopause?

A

Time period beginning 12 months after last menstrual period

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24
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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25
Q

What is the physiology of menopause?

A
  • The number of ovarian follicles decreases with age
  • This decreases ovarian function
  • Therefore, oestrogen and progesterone levels fall
  • This causes a loss of negative feedback to the gonadotropic hormones
  • Therefore, there is an increase in GnRH levels
  • This increases the levels of FSH and LH in the blood
  • This increases the frequency of anovulatory cycles
  • The end result is ovarian function eventually stops
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26
Q

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

A

Vasomotor symptoms:

  • Hot flushes
  • Night sweats

Atrophic features:

  • Vulvovaginal atrophy - dryness, pruritus, dyspareunia (due to decreased oestrogen = can cause dyspareunia)
  • Breast tissue atrophy
  • Urinary atrophy - dysuria, frequency, urgency, UTIs

Psychological symptoms:

  • Depressed mood
  • Anxiety
  • Irritability
  • Mood swings
  • Lethargy
  • Loss of libido
  • Sleep disturbance
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27
Q

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

A
  • Osteoporosis = inc risk of fracture (esp Colles’, hip, vertebrae)
  • Cardiovascular disease
  • Breast cancer
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28
Q

Menopause is primarily a clinical diagnosis. However, what investigations may be required?

A
  • FSH levels - only helpful if ?diagnosis (eg <40yr) and levels in menopausal range (raised FSH is not diagnostic for menopause but a high level indicates a lack of ovarian response)
  • Testosterone + prolactin - normal range
  • TFTs to rule out hyperthyroidism
  • Blood glucose - diabetes can cause similar symptoms
  • DEXA scan

UNHELPFUL TESTS = LH, estradiol, progesterone

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29
Q

How can you manage the various symptoms of menopause?

A

· Hot flushes - avoid triggers, regulate environmental temperature, fluoxetine/citalopram

· Insomnia - exercise, relaxation techniques

· Osteoporosis - smoking cessation, vitamin D intake, weight-bearing exercise

· Vaginal dryness - lubricants/moisturisers

Vaginal atrophy - topical oestrogen creams (estriol)

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30
Q

What is defined as premature menopause?

How common is it?

A

Menopause <40 year

20% of women

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31
Q

What are some causes of premature menopause?

A

Often no cause found (idiopathic)

Primary ovarian insufficiency:

  • Chromosome abnormalities
  • FSH receptor gene polymorphism /PCOS
  • Enzyme deficiencies
  • Autoimmune disease
  • Smoking - major risk factor
  • Infectious diseases

Secondary causes:

  • Chemo / radiotherapy
  • Bilateral oophorectomy or surgical menopause
  • Hysterectomy without oopherectomy
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32
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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33
Q

What is the management of premature menopause?

A

Oestrogen replacement needed until after average age of menopause - HRT, COCP

May have reduced fertility and require assisted conception

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34
Q

What are the main indications for HRT? (3)

A

1) Short term 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

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35
Q

What combinations of hormones are used in HRT depending on the patient?

A

Oestrogen + progestogen if no hysterectomy

Oestrogen alone if previous hysterectomy

Progesterone is added if patient has a uterus to prevent endometrial proliferation

Others:
- Tibolone = a synthetic steroid hormone that is converted to metabolites with oestrogenic, progestogenic and androgenic actions

  • Testosterone (patches and implants) to improve libido
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36
Q

What oestrogens are commonly used in HRT?

A

Estradiol
Estrone
Estriol
Conjugated quine oestrogen

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37
Q

What progesterones are commonly used in HRT?

A

17-hydroxyprogesterone

  • Dydrogesterone
  • Medroxyprogesterone acetate

19-notestosterone derivatives

  • Norethisterone
  • Levonorgestrel
38
Q

What are some benefits of HRT? (7)

A

1) Reduction in vasomotor symptoms within 4 weeks
2) QOL improvement e.g. sleep improvements
3) Improvement in mood changes
4) Improvement of urogenital symptoms within 1-3 months
(nb systemic therapy does not improve urinary incontinence)
5) Reduction of osteoporosis and fracture risk
6) Reduction in CVD risk
7) Lower risk of colorectal cancer (by 1/3rd)

39
Q

What are the main risks associated with HRT? (5)

A
  • Thromboembolic disease = VTE, PE, stroke (most likely in first year - however obesity is a greater risk factor)
  • Breast cancer - risk is reduced with short term use (<5 years)
  • Endometrial cancer
  • Gallbladder disease
  • Stress urinary incontinence
40
Q

What are some delivery routes for HRT? (6)

A
  • Continuous or cyclical oral therapy
  • Transdermal patches
  • Topical creams or gels
  • Nasal sprays
  • IUS (levonorgestrel)
  • Oestrogen releasing vaginal ring
41
Q

When is transdermal vs Oral HRT preferred?

A

Transdermal oestrogen associated with fewer risks than oral HRT

Advantageous for women with:

  • Diabetes
  • Previous VTE
  • Thyroid disorders
  • History of migraine
  • Gallbladder problems
  • Less effect on clotting factors
  • Reduce triglycerides
42
Q

When is cyclical vs continuous HRT used?

A

Cyclical if < 1yr since LMP

Continuous if:
- Used cyclical for >1yr 
OR
- >1yr since LMP
OR 
- at least 2 yrs since LMP if premature menopause
43
Q

What may happen initially to bleeding pattern with HRT? What can be done to manage bleeding issues?

A

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

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

Women with persistent vaginal bleeding >6mnths need further investigation

45
Q

Which patients require investigations prior to starting HRT and what are the investigations that should be done?

A
  • Sudden change in menstrual pattern, IMB, PCB, postmenopausal bleeding = 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
46
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

47
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

48
Q

What is endometriosis?

A

The presence of endometrial like tissue outside of the uterine cavity

49
Q

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

A

Adenomyosis

50
Q

List some common and some rare locations of endometriosis

A

Common = pelvis

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

Rare - lungs, brain, muscle, eye

51
Q

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

A

Oestrogen thus mostly affects women during their reproductive years

52
Q

What is the aetiology of endometriosis? (5 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 peritoneal cells

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

4) Impaired immunity
5) Surgical scar implantation. After a surgery, such as a hysterectomy or C-section, endometrial cells may attach to a surgical incision

53
Q

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

A

1) Dysmenorrhoea - pain starts days before bleeding and eases as period continues
2) Deep dyspareunia
3) Chronic pelvic pain - cyclical, worsens before onset of menses
4) Infertility

54
Q

Why does infertility arise in endometriosis?

A

Dense pelvic adhesions, which can lead to tubal / ovarian damage and distortion

Release of inflammatory mediators (prostaglandins) from ectopic endometrium can affect ovulation or tubal motility

55
Q

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

A

Ectopic endometrial tissue undergoes the same menstrual cycle, causing repeated inflammation which may result in the formation of adhesions

56
Q

What does deep dyspareunia in endometriosis indicate?

A

Involvement of uterosacral ligaments

57
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

58
Q

What does dysuria in endometriosis indicate?

A

Involvement of bladder peritoneum or invasion on to the bladder

59
Q

What is usually found on examination of a patient with endometriosis? However, what may be found? (5)

A

No findings on abdominal, vaginal, cervical examination (might see some visible lesions in vagina or cervix but this is rare and a sign of deep infiltrating endometriosis)

1) Adenexal masses = endometriosis ‘chocolate cysts’ or tenderness
2) Nodules/tenderness in posterior vaginal fornix or uterosacral ligaments
3) Thickening behind the uterus or adenexa
4) Fixed retroverted uterus
5) Rectovaginal nodules

60
Q

What are some complications of endometriosis? (6)

A

Fibrous adhesions causing strictures and entrapments of organs - constipation/diarrhoea
Infertility
Increased risk of ectopic pregnancy
Colonic/ureteric obstruction
Ruptured endometrioma - acute abdo pain, free fluid in pelvis
Anaemia
Malignant change

61
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

62
Q

What is the first line investigation for suspected endometriosis?

A

Transvaginal USS:

  • Endometriomas
  • Ovarian cysts (chocolate cysts)
  • However, is often normal
63
Q

What is an endometrioma?

A

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

64
Q

What is the medical management of endometriosis depending on severity of symptoms?

A

Mild to moderate pelvic pain with no complications:

  • Analgesia - NSAIDs
  • COCP - ovarian suppression
  • IUS - endometrial and ovarian suppression
  • Synthetic androgens (danazol) - ovarian suppression

Severe symptoms:

  • GnRH analoges (competitive occupancy of GnRH receptors) - ovarian suppression to induce a pseudo-menopause
  • COCP
65
Q

What is the surgical management of endometriosis?

A
  • Laparoscopic ablation of endometriotic spots
  • Laparoscopic resection of active lesions/scar tissue
  • Laparoscopic cystectomy/oophorectomy

Last resort = hysterectomy with sapling-oopherectomy

66
Q

What is pelvic inflammatory disease (PID)? What is it most common caused by?

A

General term for infection of the female upper genital tract: - Uterus (endometritis)

  • Fallopian tubes (salpingitis)
  • Ovaries (oophoritis)
  • Adjacent peritoneum (peritonitis)

Most commonly caused by ascending infection from the endocervix (STIs, BV, enteric bacteria)

Can also occur from descending infections from organs such as the appendix

67
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)

68
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

69
Q

What is the aetiology of PID?

A

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

STIs:

  • Chlamydia trachomatis = most common
  • Neisseria gonorrhoea
  • Mycoplasma genitalium

Endogenous organisms

  • Mycoplasma hominis
  • Ureaplasma urealyticum
70
Q

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

A

Increases risk of ectopic pregnancy and infertility

71
Q

What are some protective factors for PID? (2)

A

1) Barrier contraception to prevent STIs

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

72
Q

What are some signs/symptoms of PID?

A

Asymptomatic in 60% cases - diagnosis only made retrospectively during investigation of sub fertility

Symptoms

  • Bilateral lower abdominal menstrual type pain
  • Deep dyspareunia
  • Bleeding - PCB, IMB, menorrhagia, dysmenorrhoea
  • Purulent vaginal discharge
  • Fever
  • Change in bowel habit

Signs

  • Cervical motion tenderness
  • Adnexal tenderness
73
Q

What are some complications of PID? (5)

A
  • Tubo-ovarian abscess
  • Fitz-Hugh-Curtis syndrome (perihepatitis = think in women <30yr presenting with RUQ pain)
  • Recurrent PID
  • Ectopic pregnancy
  • Infertility (tubal factor)
74
Q

What is the first and most important investigation to do in someone presenting with symptoms of PID?

A

Pregnancy test - rule out ectopic pregnancy

75
Q

What is the management of PID?

A

Pain relief

Empirical antibiotic therapy - start ASAP before culture results are back + treat any sexually active young woman complaining of bilateral lower abdo pain and adnexal tenderness

  • IM ceftriaxone 500mg STAT

OR

  • Azithromycin 1g PO + doxycycline 100mg PO BD + metronidazole 400mg BD PO 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

Treat partner with doxycycline 100mg BD 7 days

76
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

77
Q

What is characteristically seen on TVUS of polycystic ovaries?

A

String of pearls

78
Q

If the patient is not seeking treatment for infertility, what are the first and second line management options for PCOS?

A

First line: weight loss via lifestyle changes e.g. diet, exercise

Second line: COCP – controls bleeding, reduces risk of unopposed oestrogen on endometrium

79
Q

If the patient is seeking treatment for infertility, what is the first line management option for PCOS?

A

First line: clomiphene citrate or letrozole to induce ovulation & weight loss if overweight

80
Q

What is the mechanism of action of clomiphene?

A

Clomiphene inhibits hypothalamic oestrogen receptors – this blocks the normal negative feedback effect of oestrogen, so there is increased secretion of GnRH from hypothalamus and increased FSH and LH from anterior pituitary which stimulate ovulation

81
Q

What may be added alongside clomiphene in the primary management of PCOS in patients seeking infertility treatment if it is ineffective alone?

A

Metformin - increases peripheral sensitivity to insulin

82
Q

If the patient is seeking treatment for infertility, what is the second line management option for PCOS?

A

Laparoscopic ovarian drilling - needlepoint diathermy in 4 places per ovary with the intent of reducing steroid hormone (FSH) production

83
Q

What are the main contraindications to HRT?

A
Undiagnosed vaginal bleeding
Breast cancer/endometrial cancer
Chronic liver disease
Hyperlipidaemia
Recent DVT/stroke
Ischaemic heart disease
84
Q

What are some DDx for acute pelvic pain?

A
  • Ectopic pregnancy
  • Rupture of ovarian cyst
  • PID
  • Ovarian torsion
  • Appendicitis
  • Strangulated hernia
  • Kidney stones
85
Q

What investigation is diagnostic of endometriosis?

A

Laparoscopy with biopsy for histological verification (gold standard):

  • 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)
86
Q

What blood marker may be raised in endometriosis?

A

CA125

87
Q

What histopathological findings are characteristic of endometriosis?

A

Gunshot lesions = black/brown nodules or cystic structures seen on serosal surfaces of ovaries + peritoneum

Salpingitis isthmica nodosa = nodular tube changes

88
Q

How would a tubo-ovarian abscess from PID present?

A
Swinging fever
Peritonitis
Systemically unwell
Palpable mass
Lack of response to treatment
89
Q

What is the best initial imaging test for ? PID? What might it show?

A

Transvaginal ultrasound scan

  • Free fluid
  • Abscesses
90
Q

How is PID primarily diagnosed?

A

Clinical findings

  • Patient history
  • Lower abdo pain
  • Cervical motion tenderness
  • Adnexal tenderness
  • Purulent vaginal discharge
91
Q

What investigation is indicated in ambiguous cases of PID?

A

Exploratory laparoscopy

92
Q

What testing must be done for all patients with possible PID?

A

STI testing
• NAAT from a vulvovaginal swab (VVS) for chlamydia, gonorrhoea and trichomonas
• Endocervical swab for gonorrhoea culture – for sensitivities as there is rising resistance to treatment
• Bloods for HIV and syphilis
• Microscopy for BV and endocervical pus in a level 3 sexual health centre
• Negative results for these does not exclude PID