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Gynaecology 2 Flashcards

1
Q

One of the VIN types is associated with older women, lichen sclerosus and greater risk of malignant progression. Which is it?

A

Differentiated type VIN

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2
Q

2 common symptoms of VIN?

A

Pain

Pruritis vulvae

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3
Q

What histological type are most vulval cancers?

A

SCC

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4
Q

What features of vulval cancer are more suggestive of malignancy than of VIN?

A

Pruritis
Bleeding (older women PMB), PCB
Discharge

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5
Q

Is most vaginal malignancy primary or secondary?

A

Secondary from endometrium, cervix or vulva

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6
Q

Vaginal cancer that is more common in teenagers and associated with maternal DES in pregnancy?

A

Clear cell adenocarcinoma

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7
Q

3 broad types of prolapse?

A

Anterior wall
Apical
Posterior wall

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8
Q

Subdivisions of anterior wall prolapse?

A

Cystocoele
Urethrocoele
Cystourethrocoele

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9
Q

Subdivisions of apical prolapse?

A

Uterine
Cervical
Upper vaginal

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10
Q

Subdivisions of posterior wall prolapse?

A

Rectocoele

Enterocoele (pouch of Douglas) - often has bowel in

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11
Q

RFs for prolapse?

A

Parity - vaginal delivery, instrumental, long second stage, big babies
Age and menopause (low oestrogen so low collagen)
Connective tissue disorders e.g. Ehlers danlos
Spins bifida occulta
Raised IAP - obesity, chronic cough, heavy lifting
Iatrogenic mostly surgical - hysterectomy

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12
Q

What is procidentia?

A

Complete prolapse and vaginal eversion

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13
Q

What is the word for complete prolapse?

A

Procidentia

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14
Q

Stage 0-4 of Pelvic Organ Prolapse Quantification grading? Based upon position of distal portion on straining.

A 
Stage 0 = normal
Stage 1 = >1cm above hymen
Stage 2 = less than 1cm either side of hymen
Stage 3 = >1cm below hymen
Stage 4 = fully everted (procidentia)
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15
Q

Management of prolapses?

A

Conservative - lose weight, quit smoking/stop cough etc
Medical - ring pessaries/shelf pessary
Surgical - sacrocolpopexy, uterine sling etc

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16
Q

With which form of incontinence is prolapse often coexistent but not necessarily related?

A

Stress incontinence

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17
Q

What is the pathophysiology behind stress incontinence?

A

Increased intra abdominal pressure with a weakened pelvic floor so bladder pressure > upper urethral pressure and sphincter leaks

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18
Q

How is stress incontinence diagnosed?

A

UTI to rule out infection + urodynamics to rule out overactivity (urge) incontinence

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19
Q

Management of stress incontinence?

A

Physiotherapy - pelvic floor training exercises for > 3m
Medical - SSRI (duloxetine) for mod-severe
Surgery if the above fail and significantly affecting QoL (TVT)

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20
Q

How does urge/overactivity incontinence tend to present?

A

Urgency usually with frequency and nocturia

In the absence of proven infection

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21
Q

How is urge/overactivity incontinence diagnosed?

A

Via cystometry Urodynamics - needs confirmed detrusor overactivity

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22
Q

What are common causes of urge/overactivity incontinence?

A

Normally idiopathic - can be nervous system dysfunction

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23
Q

Which type of incontinence can be associated with UTIs, medications and caffeine/alcohol?

A

Urge/overactivity

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24
Q

What is mixed incontinence a combination of?

A

Stress and urge

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25
Q

Management of overactivity/urge incontinence?

A

Conservative - avoid triggers, caffeine etc and keep bladder diary
Bladder training + Anticholinergics e.g. Oxybutinin, tolterodine to suppress Detrusor activity
Topical oestrogens
Injected Botulinum toxin A (BTX) to paralyse Detrusor

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26
Q

What type of incontinence is associated with chronic retention or detrusor underactivity?

A

Overflow

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27
Q

What type of incontinence can have heavy and constant flow?

A

Chronic retention/overflow -> total

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28
Q

Causes of overflow incontinence?

A

Bladder cancer
Prostate increased size
Constipation
Detrusor underactivity - DM or neuropathies

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29
Q

What are the 2 types of VIN and which is most common? Which is associated with lichen sclerosus?

A 
Usual type (most common)
Differentiated type (associated with lichen sclerosus)
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30
Q

In whom is endometriosis most common?

A

Nulliparous women closer to the menopause

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31
Q

What hormones does endometriosis growth depend on?

A

Oestrogen +/- progesterone

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32
Q

What are chocolate cysts?

A

Blood-filled endometriosis pockets

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33
Q

How does a frozen pelvis form from endometriosis?

A

Inflammation -> fibrosis and scarring -> adhesions

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34
Q

Key symptoms of endometriosis?

A

Cyclical chronic pelvic pain - just before menstruation (secondary dysmenorrhea)
Subfertility
Deep dyspareunia
Dyschezia and dysuria during menses

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35
Q

What Bimanual examination finding is suggestive of severe endometriosis with adhesions?

A

Retroverted immobile uterus + tenderness

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36
Q

What investigation differentiates between active lesions and chronic ones for endometriosis?

A

Laparascopy
Active lesions = red vesicles/petechial marks
-> white brown when less active

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37
Q

What investigation is best for adenomyosis?

A

MRI

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38
Q

What is an endometrioma?

A

Endometriotic ovarian lesion - risk of cancerous progression

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39
Q

Medical treatment for endometriosis if symptomatic?

A

Hormonal - COCP/cyclic Progestogens
GnRH analogues -> add back HRT
IUS will reduce menstrual symptoms

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40
Q

What is chronic pelvic pain?

A

Pain lasting over 6 months and not exclusively related to menstruation or sex

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41
Q

Differentials for chronic pelvic pain: cyclical vs non-cyclical?

A

Cyclical: endometriosis, adenomyosis

Non-cyclical: IBS, interstitial cystitis, chronic PID, pelvic mass

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42
Q

Appropriate management of chronic pelvic pain?

A

Analgesia
COCP if cyclical and fertility not desired
Laparoscopy to investigate

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43
Q

Why are prepubescent and postmenopausal women more susceptible to UTI and genital tract infection?

A

Lower oestrogen so thinner atrophic vaginal epithelium and increased vaginal pH (so lactobacilli aren’t as efficient vs infection)

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44
Q

Common causes of endometritis?

A

Instrumentation of uterus

Complication of pregnancy e.g. PPROM, post CS, miscarriage, ToP

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45
Q

Presentation of endometritis?

A

Persistent, heavy, painful vaginal bleeding
Tender uterus, often open os
Fever, sepsis

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46
Q

What is acute PID/salpingitis?

A

Ascending pelvic infection, often sexual although occasionally descendant from appendix

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47
Q

What infection often precedes or coexists with salpingitis?

A

Endometritis

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48
Q

What is heavily protective against salpingitis to the extent that it almost never occurs during this?

A

A viable intrauterine pregnancy

Less protective are COCP and IUS

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49
Q

Under what circumstances may acute PID go unnoticed?

A

Particularly gonococcal infection

If no coexistent endometritis

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50
Q

Symptoms of acute PID/salpingitis (particularly gonococcal)?

A

Bilateral lower abdominal/pelvic pain
Deep dyspareunia
Discharge
O/E cervical excitation, lower abdo rebound tenderness and adnexal tenderness

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51
Q

What is the role of pelvic US in acute PID?

A

Looking for abscess formation or ovarian cysts

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52
Q

What infection is associated strongly with Fitz Hugh Curtis syndrome?

A

Chlamydia

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53
Q

In whom is chlamydia more commonly symptomatic?

A

Men - 50% symptomatic, only 20% of women

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54
Q

What complication of chronic PID can result in subfertility?

A

Hydro/pyosalpinx due to Fallopian tube adhesions

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55
Q

Definition of subfertility?

A

Failure to conceive after 1 year of regular unprotected sex

Affects 15% of couples

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56
Q

Primary vs secondary failure to conceive?

A 
Primary = never conceived
Secondary = previously conceived (even if not delivered)
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57
Q

4 broad areas of causes of subfertility?

A

Egg production
Male factor
Fertilisation incl tubal factor and sexual problems
Idiopathic

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58
Q

What are the most common causes of subfertility?

A

Ovarian dysfunction or idiopathic

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59
Q

Physiological subfertility in terms of egg production?

A

Egg genetic quality decreases with age so natural reduction in fertility as women get closer to the menopause (declines from roughly age 30)

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60
Q

What is mittelschmerz?

A

Pain +/- discharge and spotting around time of ovulation (day 13-14)

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61
Q

When is body temperature lowest in the ovarian cycle?

A

Just pre-ovulation, before rising in luteal phase

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62
Q

3 tests for ovulation (apart from proof I.e. Conception)?

A

Mid-luteal phase serum progesterone (elevated = ovulated)
USS (time consuming)
OTC wee sticks for LH to predict surge

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63
Q

5 broad areas of causes of anovulation?

A

Thyroid - Hypothalamic hypogonadism
Pituitary - hyperprolactinaemia
Ovarian - PCOS, Premature ovarian failure, gonadal dysgenesis
Other e.g. Thyroid or androgen secreting tumours

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64
Q

What is the mechanism behind hypothalamic hypogonadism?

A

Reduced GnRH production -> reduced LH, FSH and oestrogen

-> anovulation

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65
Q

What is Kallmann’s syndrome?

A

Non-development of GnRH secreting neurones

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66
Q

What medication can be given to induce ovulation in PCOS? Caveats?

A

Clomifene citrate

Weight and lifestyle should be controlled first

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67
Q

What is ovarian hyperstimulation syndrome?

A

Side effect of IVF/GnRH agonists -> overstimulation of follicles which become large and painful and produce mega oestrogen
Can be fatal via hypovolaemia, electrolyte imbalance, ascites, VTE, pulmonary oedema

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68
Q

What condition is a major risk factor for OHSS particularly following clomifine use?

A

PCOS

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69
Q

What age of women are more susceptible to OHSS and why?

A

Younger women with higher follicular reserve

70
Q

Typical presentations of OHSS?

A

4-5 days following egg harvest; abdo pain and distension due to fluid ascites, nausea and vomiting, pleural effusions (SOB), hypovolaemia -> VTE, reduced UO

71
Q

What 2 things does spermatogenesis depend on?

A

LH -> testosterone production in Leydig cells

FSH -> + testosterone make Sertoli cells produce and transport sperm

72
Q

What is asthenospermia?

A

Poor sperm motility

73
Q

5 common causes of abnormal semenalysis?

A 
Idiopathic oligo/asthenozoospermia
Drugs, chemicals, smoking, alcohol
Varicocoele 
Antisperm antibodies - common post-vasectomy reversal
Infection - mumps orchitis, epididymitis
74
Q

What is another name for Kallmann’s syndrome?

A

Hypogonadotrophic hypogonadism

75
Q

Genetic causes of sperm abnormalities?

A

Klinefelters XXY

CF

76
Q

3 common causes of tubal dysfunction?

A

Infection - PID
Endometriosis
Surgery/adhesions

77
Q

What are the 2 main methods for investigating tubal damage?

A

Lap and Dye

Hysterosalpingogram - less invasive and safer but may not show endometriosis or adhesions

78
Q

2 methods for intrauterine insemination?

A

In line with cycle (LH)

GnRH ovulation induction (stimulated IUI)

79
Q

What are the requirements for IUI?

A

Patent tubes and no ovarian problems

80
Q

What does ICSI stand for and what assisted contraception method is it used in conjunction with?

A

Intracyctoplasmic Sperm Injection, oft used with IVF when indication is male factor infertility

81
Q

What is the primary indication for IVF?

A

Tubal or idiopathic with confirmed ovulatory reserve via FSH/AMH

82
Q

What are 3 methods of assessing ovarian reserve?

A

FSH (high = low reserve)
AMH (high = high reserve)
TVUS of ovaries to measure antral follicle count AFC

83
Q

What technique associated with IVF may be useful for older women or those at higher risk of chromosomal abnormalities e.g. CF?

A

Preimplantation Genetic Diagnosis PGD

84
Q

What are the best methods of contraception for use in adolescents?

A

Pill and condoms for STI protection
Depo-provera (risk of reduced bone density)
Emergency contraception

85
Q

What long term risk does depo-provera carry, particularly in younger people?

A

Osteoporosis

86
Q

What methods of contraception are recommended for those with IBD or other malabsorbative disorders?

A

Oral contraception use limited due to reduced absorption so alternatives e.g. Patch, injection, implants
Increased risk of osteoporosis anyway so avoid Depo-provera

87
Q

Contraception suitable for those breastfeeding?

A

In theory breastfeeding is contraceptive in itself as it inhibits ovulation
However if using added contraception: avoid COCP but POP is fine
IUD fine from 4 weeks postpartum

88
Q

Rules for contraception for women around the time of menopause?

A

Women under 50 should use contraception for > 2years post LMP
Women over 50 should use contraception for > 1 year post LMP
IUS can be particularly useful for those with excessive menstrual loss

89
Q

How do combined oestrogen and progesterone contraceptives work?

A

Negative feedback loop - suppress LH and FSH via GnRH and thus inhibit ovulation
Also thin endometrium and thickens cervical mucus (progesterone)

90
Q

What is the normal regime for COCP?

A

3 weeks on -> bleed due to prog withdrawal -> 1 week off

91
Q

Major contraindications to COCP?

A 
VTE, CV Hx
Migraine with aura
Active breast or endometrial cancer
Thrombophilias + liver disease 
Pregnancy
Most smokers
Really high BMI
92
Q

Apart from contraceptive use, what is the COCP useful for?

A

Cycle control - menorrhagia, dysmenorrhea, irregular periods
Acne and hirsutism
Simple ovarian cysts

93
Q

What 3 conditions can the COCP be used to suppress?

A

Fibroids
Endometriosis
PID/ovarian cysts

94
Q

What are some considerations to make when considering COCP usage?

A

Compliance/missed pill
Reduced absorption
Liver enzyme inducers e.g. Anticonvulsants
Major surgery (stop 4 weeks before)
STI risk (concurrent condom use in teens and young adults)

95
Q

4 major side effects of the COCP?

A

Nausea
Headache
Breast pain
Weight gain

96
Q

How does the POP work?

A

By inhibition of cervical mucus and preventing uterine proliferation - inhibit ovulation in 50%

97
Q

4 progestogenic side effects?

A

Vaginal spotting (breakthrough bleeds)
Pre-menstrual syndrome
Weight gain
Breast pain

98
Q

What can the POP cause if it doesn’t result in anovulation (as in 50%)?

A

Functional ovarian cysts (follicular or luteal)

99
Q

In whom is the POP>COCP?

A

In older women

In those who the COCP is contraindicated

100
Q

2 types of Long Acting Reversible Contraceptives LARCs?

A

Depo provera - progesterone injection

Progestogen implant rod

101
Q

How do the LARCs work and what do they therefore protect against?

A

Work by preventing ovulation and so protect against functional ovarian cysts and ectopics

102
Q

Why is the progestogen rod implant a better choice than depo for teenagers and those with IBD?

A

Doesn’t cause a reduction in bone density so no risk osteoporosis

103
Q

2 options for emergency contraception?

A

Morning after pill or IUD

104
Q

What 2 morning after pill options are there?

A

Levonelle - up to 3 days after sex

Ulipristal (ellaOne) - up to 5 days after sex

105
Q

When can an IUD be fitted after unprotected sex as emergency contraception?

A

Up to 5 days after sex or 5 days after expected date of ovulation

106
Q

Potential complications of IUD/IUS insertion?

A 
Pain/cervical shock due to increased vagal tone after insertion
Threads disappearing
IUD may worsen dysmenorrhea/menorrhagia
Infection and PID 
Ectopic pregnancy
107
Q

Which type of IUD can worsen menstrual symptoms?

A

Copper coil IUD

108
Q

What are 2 causes of threads disappearing from IUD/IUS insertion?

A

Expulsion

Perforation of uterine wall

109
Q

Average age of menopause?

A

51

110
Q

When is the menopause officially recognised?

A

12 months after LMP

111
Q

Define the perimenopause?

A

From onset of symptoms to 1 year after LMP

112
Q

What is premature menopause? What does it require?

A

Ovarian failure before age of 40

Requires HRT until at least age of 50

113
Q

What is PMB defined as?

A

Bleeding occurring >1 year after LMP

114
Q

What are 3 important causes of PMB to rule out?

A

Endometrial cancer/hyperplasia with atypia
Intrauterine polyps
Cervical cancer

115
Q

4 other potential causes of PMB?

A

Withdrawal bleeds with sequential HRT
Atrophic vaginitis
Cervicitis or cervical polyps
Ovarian carcinoma

116
Q

What must purulent blood stained discharge be assumed to be until proven otherwise?

A

Endometrial carcinoma

117
Q

Appropriate line of investigations for PMB?

A

Physical examination + smear test

TVUS -> endometrial pipelle biopsy -> hysteroscopy

118
Q

5 areas of symptoms of the menopause?

A

Cardiovascular - stroke and MI risk
Vasomotor - hot flushes, night sweats (-> sleep disturbance)
Urogenital - vaginal atrophy, dyspareunia, itching burning dysuria, urinary frequency, urgency, Nocturia, incontinence and infection
Sexual and psychological - loss of interest and arousal, dyspareunia, irritability, mood changes, depression, sleep disturbance
Osteoporosis

119
Q

Lines of investigation for the menopause?

A

FSH
AMH
T4/TSH, LH, oestrogen, progesterone

120
Q

When investigating anovulation, what low level of hormone indicates anovulation?

A

Low progesterone

121
Q

General rules for types of HRT requirement?

A

Oestrogen only if no uterus

Oestrogen and progesterone for uterus

122
Q

Combined HRT regimes?

A 
Quarterly or monthly bleeds (prog given sequentially)
No bleeds (prog given continuously e.g. IUS)
123
Q

Which HRT method is the best for protecting vs endometrial cancer?

A

Continuous ie no bleed, as it induces endometrial atrophy

124
Q

3 benefits of HRT?

A

Reducing troublesome symptoms
Reducing osteoporosis risk
Reducing colorectal cancer risk

125
Q

4 potential risks of HRT?

A

Increased risk of endometrial cancer if oestrogen only and uterus present
Increased risk of breast cancer if combined
Increased risk of VTE particularly for oral (during 1st year)
Increased risk of gallbladder disease

126
Q

What medications might be useful for perimenopausal symptoms for those wanting to avoid oestrogen (e.g. Breast ca risk)?

A

Progestogens

SSRIs for vasomotor

127
Q

What is a miscarriage and when do most occur?

A

Fetus dies or delivered dead before 24 weeks

Most occur before 12 weeks

128
Q

6 types of miscarriage?

A 
Threatened
Inevitable
Complete
Incomplete
Septic
Missed
129
Q

What indicates a threatened miscarriage?

A

Bleeding PV, closed cervical os. Fetus is still alive and correct size for dates

130
Q

What fraction of people with threatened miscarriage go on to miscarry?

A

1/4

131
Q

What indicates an inevitable miscarriage?

A

Heavier PV bleeding and open cervical os

132
Q

What indicates an incompletely miscarriage?

A

Some but not all of fetal parts are passed; cervical os still open

133
Q

What indicates a complete miscarriage?

A

All fetal parts have been passed and the cervical os is closed

134
Q

What indicates septic miscarriage?

A

Uterine contents infected -> endometritis. Patient will have offensive vaginal loss with a tender uterus +/- systemic infection

135
Q

What indicates a missed miscarriage?

A

Fetur not developed/died in utero but not recognised until bleeding or US
Small for dates fetus and closed os

136
Q

What types of miscarriage present with an open os?

A

Incomplete

Inevitable

137
Q

What types of miscarriage present with a closed os?

A

Threatened
Complete
Missed

138
Q

What are sporadic miscarriages usually caused by?

A

Isolated chromosomal or genetic abnormalities

139
Q

What are ‘recurrent miscarriages’ and why do they most commonly occur?

A

3 or more miscarriages in succession
Antiphospholipid Abs (thrombosis in placental circulation)
Parental chromosomal defects
Anatomical factors

140
Q

Appropriate investigations for possible miscarriage (bleeding PV)?

A

US to observe viable IUP or retained fetal products
HCG levels
FBC and rhesus

141
Q

What hCG levels are indicative of viable IUP or miscarriage?

A

Increase of >66% in 48 hours is indicative of viable IUP

Plateauing or decreasing suggests viable IUP

142
Q

What investigations are combined to assess possibility of ectopic pregnancy?

A

HCG - if rise of >66% in 48 hours but no visible IUP suggests ectopic
Visualisation of IUP normally rules out ectopic

143
Q

What is a heterotopic pregnancy?

A

IUP + ectopic pregnancy together

144
Q

Under what circumstances does anti-D need to be given for miscarriage?

A

For bleeding > 12 weeks or surgically/medically managed in rhesus negative women

145
Q

Management methods for non-viable IUP?

A

Expectant - for incomplete or inevitable miscarriage and no signs of infection
Medical - prostaglandins possibly with preceding mifepristone
Surgical - ERPC for infection, heavy bleeding or maternal choice

146
Q

What is Asherman’s syndrome?

A

A rare complication of ERPC and some uterine surgical procedures resulting in amenorrhea due to outflow blockage

147
Q

When do rhesus negative women need to be given anti-D for ToP?

A

Within 72 hours of ToP

148
Q

When is medical ToP most appropriate?

A

Less than 7-9 weeks

From 13-24 weeks

149
Q

When is surgical ToP most appropriate?

A

7-13 weeks

150
Q

What is the most common area for ectopic pregnancy?

A

Fallopian tubes

Occasionally Cornu, cervix, ovary, intra-abdo

151
Q

RFs for ectopic pregnancy?

A

Previous ectopic
Tubal - PID, surgical adhesions
Increasing maternal age
Smoker

152
Q

What should a patient who conceives despite IUD in situ be assumed to have until proven otherwise?

A

Ectopic pregnancy

153
Q

Presentation for ectopic pregnancy?

A 
Lower abdo pain - colicky then chronic
Scanty dark vaginal bleeding
Abdo/rebound tenderness
Adnexal tenderness, cervical excitation
Small uterus for dates, closed os
154
Q

What should all women of reproductive age who present with bleeding, pain or collapse have done?

A

Pregnancy test

155
Q

Medical management of ectopic pregnancy?

A

If unruptured, stable patient and hCG

156
Q

Surgical management of ectopic pregnancy?

A

Laparoscopy and salpingectomy/salpingostomy if subacute

Laparotomy and salpingectomy if acute

157
Q

What is hyperemesis gravidarum?

A

Nausea and vomiting in early pregnancy so severe as to cause dehydration, weight loss or electrolyte disturbance

158
Q

In whom is hyperemesis more common?

A

Older, multiparous women
UTI
Molar pregnancy

159
Q

When does hyperemesis normally resolve by?

A

12-14 weeks

160
Q

Management of hyperemesis?

A

IVT +/- antiemetics e.g. Cyclizine, metoclopramide, ondansetron

161
Q

What vitamin needs to be given in hyperemesis?

A

B particularly thiamine to prevent wernicke-korsakoff

162
Q

What is gestational trophoblastic disease GTD?

A

Trophoblastic tissue which normally invades the endometrium proliferates more aggressively than normal -> mega hCG levels

163
Q

What is local, non-invasive trophoblastic overproliferation called?

A

Molar pregnancy - hyatidiform mole

164
Q

2 types of hyatidiform mole?

A

Complete (no fetus, entirely paternal)

Partial (+/- fetus, usually triploid)

165
Q

What is a locally invasive GTD called and what does it have the potential to do?

A

Invasive mole

Can metastasise and become a choriocarcinoma

166
Q

What is persistently elevated hCG in the context of GTD called?

A

Gestational trophoblastic neoplasia GTN

167
Q

In whom is GTD more common?

A

Asian women at extremes of reproductive age

168
Q

How does GTD present?

A

Large uterus, possible heavy vaginal bleeding
Early pre-eclampsia and hyperthyroidism
Hyperemesis

169
Q

What does a ‘snowstorm’ uterus on US indicate?

A

Complete moles

170
Q

Management of GTD?

A

ERPC + histological diagnosis

Serum or urine hCG follow up to rule out malignancy

Revision Qs (28 decks)

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