Gynaecology Pt. 2 Flashcards

1
Q

What are some infective causes of vaginal discharge?

A
  • Bacteria vaginosis
  • Vulvovaginal candidiasis
  • Trichomoniasis
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2
Q

What is bacterial vaginosis?

A
  • MOST COMMON cause of abnormal vaginal discharge
  • Occurs in 5-50% of women worldwide
  • Definitive cause is not known but thought to be associated with depletion of lactobacilli dominant in the healthy vaginal flora
  • Vaginal pH will also rise > 4.5
  • Presence of vaginal epithelial biofilm consisting of Gardnerella vaginalis has also been described
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3
Q

What are risk factors of having bacterial vaginosis?

A
  • Douching
  • Afro-Caribbean
  • Smoking
  • Having a new sexual partner
  • Receiving oral sex
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4
Q

What are symptoms of bacterial vaginosis?

A
  • Offensive vaginal discharge (‘fishy’ odour)

- Homogenous off-white vaginal discharge with a high pH

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5
Q

How is bacterial vaginosis diagnosed?

A
  • Evaluation of Gram-stain of vaginal discharge using validated method (e.g. Hay-Ison, Nugent or Amsels criteria)
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6
Q

What conditions are associated with bacterial vaginosis?

A
  • PID
  • Posthysterectomy vaginal cuff cellulitis
  • Pregnancy: preterm birth, rupture of membrane and miscarriage
  • Increased risk of HIV acquisition
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7
Q

What is the management of bacterial vaginosis?

A
  • Oral or intravaginal treatment with metronidazole or clindamycin
  • Advice: vaginal douching and excessive genital washing should be avoided
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8
Q

What is vulvovaginal candidiasis?

A
  • When Candida yeast (usually C. albicans) causes vulval and vaginal inflammation
  • The vagina is colonised by Candida sp. in up to 20% of women in their reproductive years and 40% of pregnant women
  • Usually ASYMPTOMATIC
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9
Q

What are the symptoms of vulvovaginal candidiasis?

A
  • Itching
  • Irritation
  • White, curdy vaginal discharge
  • Erythema, oedema and fissuring of the vulva and vagina (on examination)
  • NOTE: symptoms may be more frequent and persistent if diabetic, immunocompromised or pregnant
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10
Q

How is vulvovaginal candidiasis diagnosed?

A
  • Bacterial swab for microscopy and culture
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11
Q

What is the management of vulvovaginal candidiasis?

A
  • Prescribe antifungal treatment
    • Most women: intravaginal antifungal cream or pessary (clotrimazole, econazole, miconazole) or an oral antifungal (fluconazole, itraconazole)
    • Women > 60 years: oral antifungals may be more acceptable because of ease of administration
    • Girls aged 12-15 years: consider prescribing topical clotrimazole 1% or 2% applied 2-3 times per day (do NOT prescribe intravaginal or oral antifungal)
    • Breastfeeding women: intravaginal clotrimazole or oral fluconazole
    • If vulval symptoms: topical imidazole (clotrimazole, ketoconazole) in addition to an oral or intravaginal antifungal
    • NOTE: intravaginal clotrimazole (Canesten), oral fluconazole and topical clotrimazole can be purchased OTC
  • Advice
    • Return if symptoms have not resolved in 7-14 days
    • Avoid predisposing factors:
      • Washing and cleaning the vulval area with soap or shower gels , wiped and feminine hygiene products
      • Cleaning the vulval area more than once per day
      • Washing underwear in biological washing powder and using fabric conditioners
      • Vaginal douching
      • Wearing tight-fitting and/or non-absorbent clothing
    • Wash the vulval area with a soap substitute - used externally and not more than once per day
    • Use simple emollient to moisturise vulval area
    • Consider probiotics (e.g. live yoghurts) orally or topically to relieve symptoms
  • Do NOT routinely treat asymptomatic sexual partner
    • Male partner could get candida balanitis
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12
Q

What is Trichomoniasis?

A
  • Vaginal and urethral infection caused by flagellate protozoan Trichomonas vaginalis (TV)
  • TV is sexually-transmitted, therefore, simultaneous treatment of current and recent sexual partners is required
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13
Q

What are the symptoms of Trichomoniasis?

A
  • Vaginal discharge with a variable appearance
  • Symptoms of vulvo-vaginitis
  • Asymptomatic infection is seen in up to 50% of women and their male partners
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14
Q

How is trichomoniasis diagnosed?

A
  • Testing is required if symptomatic
  • NAAT (nucleic acid amplification test) on vaginal or endocervical swab or urine
  • Some test swill also be able to detect N. gonorrhoea or Chlamydia trachomatis on the same swab (ideally vulvovaginal swab)
  • Microscopy and culture as well as POCT (point of care test) are available but have lower sensitivity
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15
Q

How is trichomoniasis managed?

A
  • Metronidazole
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16
Q

What are causes of cervicitis and pelvic inflammatory disease?

A
  • Gonorrhoea

- Chlamydia

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17
Q

What is Gonorrhoea?

A
  • Caused by Nerisseria gonorrhoea (Gram-negative intracellular diplococcus)
  • Simultaneous treatment of current and previous sexual partners is required
  • Ascending infection may result in PID
  • Rarely, it can lead to haematogenous spread causing disseminated gonococcal infection with a purpuric non-blanching rash and/or arthralgia (usually monoarticular in a weight-bearing joint)
  • Ophthalmic infection can occur due to inoculation from infected genital secretions
  • Neonatal infection may occur when the mother has endocervical infection a the time of delivery
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18
Q

What are the symptoms of Gonorrhoea?

A
  • Endocervical infection is ASYMPTOMATIC in up to 50%
  • Altered vaginal discharge (MOST COMMON)
  • Lower abdominal pain
  • Rectal infection (through transmucosal spread or receptive anal sex)
  • Pharyngeal infection (through receptive oral sex)
  • This is nearly always asymptomatic
  • Examination is often normal (cervicitis with or without mucopurulent discharge may be seen)
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19
Q

How is Gonorrhoea diagnosed?

A
  • Required if symptomatic of if the woman has another STI
  • NAAT is the gold standard
  • If N. gonorrhoea is identified, a sample should be obtained for culture and sensitivity (because there is widespread resistance)
  • Screening for other STIs (particularly chlamydia) is important because dual infection is common
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20
Q

How is Gonorrhoea managed?

A
  • Ceftriaxone IM
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21
Q

How is dual infection (gonorrhoea and chlamydia) managed?

A
  • Parenteral 3rd generation cephalosporin (e.g. ceftriaxone) + azithromycin
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22
Q

What is Chlamydia?

A
  • MOST COMMON bacterial STI
  • Women < 25 years are most frequently affected
  • Caused by Chlamydia trachomatis
  • Often asymptomatic
  • May cause subclinical PID and complications
  • Screening programmes have been developed for the highest risk age group
  • Examination is often NORMAL
  • Cervicitis with mucopurulent discharge may be observed
  • Neonates born to mothers with cervical chlamydia infection may develop conjunctivitis
  • Reactive arthritis is a complication but is more common in men
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23
Q

What are the risk factors of chlamydia?

A
  • New sexual partner
  • Altered vaginal discharge
  • Intermenstrual or post-coital bleeding
  • Abdominal pain
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24
Q

How is chlamydia diagnosed?

A
  • NAAT (some test N. gonorrhoea simultaneously)

- Best specimen is a vulvovaginal swab that may be self-taken

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25
Q

What is the management of chlamydia?

A
  • Azithromycin or doxycycline are equally effective

- Simultaneous treatment of current and recent sexual partners

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26
Q

What is Pelvic Inflammatory Disease?

A
  • Occurs when there is ascending infection from the endocervix to the higher reproductive tract
  • Recognised complication of chlamydia
  • Occurs less frequently with gonorrhoea
  • Other implicated organisms include Mycoplasma genitalium and vaginal microflora
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27
Q

What are the symptoms of PID?

A
  • Lower bilateral abdominal pain
  • Dyspareunia
  • Altered vaginal discharge
  • Abnormal vaginal bleeding (intermenstrual or post-coital)
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28
Q

What are the signs of PID?

A
  • Lower abdominal and cervical motion tenderness

- Cervicitis

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29
Q

What are the investigations for PID?

A
  • Testing for all STIs
  • Exclusion of pregnancy
  • Laparoscopy may reveal scarring and adhesions between structures in the pelvis and the development of hydrosalpinges
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30
Q

What is the management of PID?

A
  • IMPORTANT: if an IUD is in situ, consider removal although the risk of pregnancy if there has been unprotected sex in the last week should be considered
  • Macrolide (e.g. azithromycin) OR tetracycline (e.g. doxycycline) AND metronidazole with a parenteral 3rd generation cephalosporin
  • Sexual partners require screening and empirical treatment (usually azithromycin)
  • Provide women with information regarding possible sequelae
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31
Q

What are genital herpes?

A
  • TWO types:
    • HSV1 (orolabial herpes)
    • HSV2 (genital herpes
  • The virus establishes latency in the local sensory ganglia and may reactive leading to viral shedding with or without symptoms
  • Primary infection = first infection
  • Most initial infections are asymptomatic (but can still be infectious)
  • Recurrence rates are higher with HSV2
  • Recurrence rates reduce in frequency with time
  • Neonatal herpes is devastating and has a mortality of up to 30% and lifelong neurological morbidity in 70%
  • C-section is recommended for women with first-acquisition genital herpes in the 3rd trimester
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32
Q

What are the symptoms of genital herpes?

A
  • Genital pain
  • Dysuria
  • Multiple superficial tender ulcers with regional lymphadenopathy
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33
Q

How are genital herpes diagnosed?

A
  • Detection of the virus from the genital lesions by gently taking a swab
  • PCR is the test of choice
  • Type-specific serology (for IgG and IgM to HSV1 and 2) can be useful to establish whether the infection is primary, non-primary or recurrence
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34
Q

How is genital herpes managed?

A
  • Aciclovir (or valaciclovir)
    • Safe in pregnancy
  • Most effective if given as soon as possible after symptoms begin
  • Important information for patients: lifelong nature of infection, asymptomatic shedding, risk to sexual partners, need for disclosure, effectiveness of condoms and antivirals in limiting transmission
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35
Q

What are genital warts?

A
  • Benign epithelial tumours caused by HPV infection
  • Over 100 genotypes
  • Types 6 and 11 cause 90% of genital warts
  • Majority of cases are subclinical
  • Types 16 and 18 are also spread through sexual contact but cause anogenital dysplasia and cancer rather than warts
  • HPV vaccination is available in a bivalent (16 and 18) and quadrivalent (6, 13, 16 and 18) form
  • VERY RARELY, infants born to mothers with HPV may develop respiratory papillomatosis (however, C-section should not be recommended)
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36
Q

How is genital warts diagnosed?

A
  • Clinical examination
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37
Q

How are genital warts managed?

A
  • Ablation with liquid nitrogen (cryotherapy)
  • Surgical techniques
  • Patient-applied topical therapies (e.g. podophyllotoxin-containing preparation, imiquimod)
  • Treatment is optional because the lesions are benign
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38
Q

What is syphilis?

A
  • Caused by Treponema pallidum
  • Spread through direct contact with secretions from infective lesions or via transplacental passage of bacteria during pregnancy
  • If untreated, it can relapse and remit leading to complications later on
  • Infectivity declines with time
  • Treatment with penicillin-based regimens are curative (but reinfection is possible)
  • More common in homosexual men
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39
Q

How is syphilis infection classified?

A
  • Acquired or congenital

- Late or early

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40
Q

What is acquired early syphilis?

A
  • First manifestation is the chancre at the site of exposure
  • This is a single genital lesion
    • NOTE: this is sometimes seen in other sites (e.g. oral cavity)
  • The lesion is typically painless, indurated and exudes serous fluid containing T. pallidum
  • Regional lymphadenopathy
  • This will resolve over a few weeks
  • Relapse may occur for up to 2 years (time limit for ‘early’ infection)
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41
Q

What is secondary syphilis?

A
  • Widespread erythematous rash typically including the palms and soles
  • Can result in alopecia, oral and genital mucous lesions and raised lesions usually in the anogential region called condylomata lata
  • Typically resolves spontaneously as the immune response controls the infection
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42
Q

What are complications of syphilis?

A
  • Meningitis
  • 8th nerve palsy leading to deafness or tinnitus
  • Ophthalmic involvement (uveitis)
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43
Q

What are the late complications of syphilis?

A
  • Gummatous lesions (granulomatous, locally destructive lesions typically affecting the skin and bone)
  • Cardiovascular involvement (usually affecting ascending aorta, resulting in aortic valve incompetence)
  • Neurological involvement
    • Meningo-vascular disease
    • Tabes dorsalis
    • Progressive dementing illness
    • General paresis
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44
Q

How is syphilis diagnosed?

A
  • Serology
  • Direct detection of T. pallidum from infectious lesions (usually dark field microscopy or PCR)
  • Non-treponemal serological tests
    • Rapid plasma reagin (RPR)
    • Venereal Disease Reference Laboratory (VDRL)
    • These show rising titres during acute, active infection that drop with time/following treatment
    • It is useful for monitoring treatment
    • May be false negative in early infection
    • May be false positive in other physiological or diseases states (e.g. pregnancy, rheumatological conditions)
  • May require confirmation using other treponemal tests, such as:
    • Enzyme or chemiluminescence immnuoassays (EIA/CLIA)
    • Treponema pallidum particle or haemagglutination assay (TPPA/TPHA)
    • These may also be negative in early disease
    • Should be repeated 4-6 weeks later if the diagnosis is still suspected
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45
Q

What is the management of syphilis?

A
  • Curative
  • Depot preparations of penicillin
  • Different regimes for different stages of infection
  • Simultaneous treatment of current sexual partners is required
  • If the time of infection is unknown, tracing and testing previous partners is important
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46
Q

What are the gynaecological complications in HIV-positive Women?

A
  • More likely to have infection with HPV 16 or 18
  • Higher incidence of CIN and high-grade squamous intraepithelial lesion (HSIL)
  • Because of this, annual cervical cytology is recommended
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47
Q

Describe contraception and preconception management in HIV-positive women

A
  • Most antiretrovirals interact with hormonal contraceptives (reduced efficacy of the contraceptive)
  • Dynamic HIV drug interaction website (University of Liverpool) provides accurate information on specific drug interactions
  • Health of HIV-positive woman and partner should be optimised prior to attempting pregnancy
  • Transmission between the partners is extremely low when the positive partner has an undetectable viral load
  • Fertility assessment of both partners is good practice
  • STI screens should be done for both partners
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48
Q

What is urge incontinence?

A
  • involuntary leakage accompanied by or immediately preceded by urgency
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49
Q

What is stress incontinence?

A
  • involuntary leakage on effort, exertion, sneezing or coughing
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50
Q

What are different types of urine voiding symptoms?

A
  • Slow stream: perception of reduced urine flow
  • Spitting or spraying: where the stream or urine is not a single flow
  • Intermittent stream: urine flow that stops and starts
  • Hesitancy: difficulty in initiating micturition resulting in a delay in the onset of voiding
  • Terminal dribble: a prolonged final part of micturition, where the flow has slowed to a trickle or dribble
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51
Q

Describe the micturition cycle

A
  • As bladder capacity is reached, sensory signals from stretch receptors in the bladder wall send the sensation of bladder filling
  • Voluntary delay of micturition until socially convenient is achieved by cortical inhibition of the spinal voiding reflex arc
  • Before voiding, this inhibition is removed leading to relaxation of the pelvic floor muscles and urethral sphincters
  • The detrusor muscle is innervated by muscarinic cholinergic nerves of the parasympathetic nervous system (leading to contraction)
  • The urethral sphincter is innervated by noradrenergic neurones of the sympathetic nervous system (causing sphincter contraction) and somatic fibres (for voluntary contraction and relaxation) from the pudendal nerves
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52
Q

What does the urethral sphincter mechanism consist of in women?

A
  • Internal sphincter - smooth muscle
  • External sphincter - striated muscle
  • In premenopausal women, the urethral epithelium has a rich blood supply and contributes to continence by acting as a seal
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53
Q

What is stress incontinence suggestive of?

A
  • An incompetent urethral sphincter
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54
Q

What is urethral sphincter weakness mainly due to?

A
  • Hypermobility
  • Pelvic floor and ligaments cannot retain the urethra in position and it falls through the urogenital hiatus during increases in abdominal pressure
  • Leads to loss of intra-abdominal pressure transmission to the urethra leading to leakage of urine
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55
Q

What is intrinsic sphincter deficiency?

A
  • Less common
  • Occurs when urethral closure pressure is low without urethral mobility
  • Caused by weakness of the sphincter muscles and loss of cushioning seal effect in the urethra
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56
Q

What urethral sphincter problems can childbirth lead to?

A
  • Stretching/damage of the pudendal nerves
  • Overstretching of the pelvic floor muscles
  • Direct muscle damage can result in loss of pelvic floor support (and urethral hypermobility)
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57
Q

What are the risk factors for stress incontinence?

A
  • Multiparity
  • Forceps delivery
  • Perineal trauma
  • Long labour
  • Epidural analgesia
  • Birthweight > 4 kg
  • Increasing age
  • Postmenopause
  • Obesity
  • Connective tissue disease
  • Chronic cough (e.g. bronchiectasis)
  • Doxazocin (alpha blocker)
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58
Q

What is detrusor overactivity?

A
  • Characterised by involuntary detrusor contractions during the filling phase of micturition
  • Women will often complain of symptoms of an overactive bladder but may not be incontinent unless urethral sphincter function is compromised or detrusor contractions are of very high pressure
  • Detrusor overactivity may be due to differences in sensory and interstitial nerves in the bladder wall and differences in neurotransmitters
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59
Q

What are modifiable risk factors of detrusor overactivity?

A
  • Obesity
  • Smoking
  • Continence surgery carries a 5-10% risk of new detrusor overactivity
  • Childhood bedwetting
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60
Q

What should be included in the history for incontinence?

A
  • Detailed history to determine whether they are symptoms of stress or urge incontinence
  • If there are mixed symptoms, assess which ones are predominant
  • Measures of severity
    • Number of episodes per day of frequency, urgency and leakage
    • Are continence pads needed?
    • If so, how many and what size?
    • Does the patient need to change underwear or outer clothes because of leakage?
    • Changes in behaviour to accommodate for this issue?
      • E.g. reduced fluid intake, limiting social activities
    • Associated symptoms
      • Prolapse
      • Faecal incontinence
      • Sexual difficulties
    • Past medical history for predisposing factors (e.g. previous surgery, medical conditions)
      • Red flags: haematuria, rectal bleeding, significant pain
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61
Q

What’s included in the examination for incontinence?

A
  • General examination
  • Abdominal and pelvic examination
  • Visible leakage during coughing or Valsalva
  • Ability of the patient to contract and hold the contraction of pelvic floor muscles is essential
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62
Q

How is incontinence investigated?

A
  • MSU
  • Bladder diary (usually about 3 days)
    • Record amount, type and frequency of drinks taken
    • Record timing, frequency and volume of voids
  • Pad test
    • Patient wears a pre-weighed sanitary pad for a variable length of time (e.g. 1 hour in clinic or 24 hours at home) whilst performing provocation tests (e.g. handwashing, climbing stairs, coughing)
    • The change in weight is a measure of the amount of urine lost
  • Pelvic or renal ultrasound if there are symptoms of pelvic pain , pelvic mass, haematuria, bladder pain or recurrent UTI
  • Discuss with the MDT (gynaecologist, urologist, continence nurse, physiotherapist and maybe medicine for the elderly consultant)
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63
Q

What are the elements of conservative management for incontinence?

A
  • Advice about fluid balance
  • Reduction of caffeine intake
  • Bladder retraining
  • Pelvic floor muscle exercise
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64
Q

Describe the management of fluid balance for urine incontinence

A
  • (avoid excessive intake > 2.5 litres)
  • NOTE: however, reducing fluid intake can result in an increased sensation of urgency due to the more concentrated urine
  • Women should be encouraged to drink 1.5-2.5 L of water per day
  • Avoid caffeinated drinks and artificially sweetened or carbonated drinks
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65
Q

Describe pelvic floor muscle exercises to help urine incontinence

A
  • The woman contracts the pelvic floor muscles by direct coaching whilst being examined vaginally to ensure correct identification of the levator muscle complex
  • Programmes are developed to increase the duration of the hold of the contraction and to increase the number of contractions that can be performed consecutively
  • This builds strength and endurance
  • This measure can lead to cure in over 50% and improvement in 75% or more
  • Adherence is a barrier to success
  • Pelvic floor exercises work for both incontinence and overactive bladder
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66
Q

What does bladder retraining involve?

A
  • Involved re-educating the patient (and her bladder) to increase the interval between voids to re-establish normal frequency
  • The urgency and fear of leakage associated with overactive bladder leads to the woman wanting to void whenever they are aware of bladder filling sensations
  • Bladder retraining involves teaching the woman about normal bladder sensation, rate of urine production and normal bladder capacity (350-500 mL)
  • The woman should be encouraged to delay voiding for several minutes after when she would normally void
  • This should be done in a step-wise fashion
  • NOTE: obesity is associated with increased risk and severity of incontinence
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67
Q

What are common urodynamic diagnoses?

A
  • Detrusor Overactivity: presence of a detrusor contraction, with or without sensation, during the filling phase of urodynamics
  • Detrusor Overactivity Incontinence: leakage from the urethra in associated with a detrusor contraction and increase in bladder pressure
  • Urodynamic Stress Incontinence: leakage from the urethra in association with a rise in abdominal pressure (e.g. coughing) without a detrusor contraction (a sign of urethral sphincter weakness)
  • Mixed Incontinence: presence of both urodynamic stress incontinence and detrusor overactivity
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68
Q

How does urodynamic testing work?

A
  • A fine pressure catheter is placed in the bladder through the urethra, and a second catheter is inserted into the rectum
  • The bladder is filled with warm saline whilst pressure recordings are made with the patient sitting on a commode that records leakage
  • Detrusor pressure = bladder pressure - abdominal pressure
  • During the filling of the bladder, the patient is asked to declare the onset of bladder filling sensation, a strong desire to void and the onset of urgency
  • When urgency is reported, filling is stopped and the patient performs various actions to provoke leakage (e.g. coughing, star jumps) before voiding
  • Urodynamic testing is reserved for patients who fail to improve with conservative measures
  • IMPORTANT: the relationships between urinary symptoms and urodynamic diagnoses is not strong
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69
Q

What is the medical treatment for incontinence?

A
  • Anticholinergic medications are the mainstay because parasympathetic nerves stimulate the detrusor muscle to contract
  • Inhibition of acetylcholine action at the muscarinic receptor also leads to reduced perceived sensations of bladder filling
  • Anticholinergic Medications
    • Oxybutynin: 2.5-5 mg up to TDS
      • 1st choice recommended by NICE
      • Modified preparations of 5 mg OD increasing weekly by 5 mg up to 20 mg daily
    • Propiverine: 15 mg 1-3/day
    • Trospium: 20 mg BD
    • Tolterodine: 2 mg BD
    • Fesoterodine: 4 mg OD (max 8 mg OD)
    • Solifenacin: 5 mg OD (max 10 mg OD)
    • Darifenacin: 7.5 mg OD
  • All anticholinergics have similar efficacy
  • Mirabegron is a new beta-3 adrenergic agonist that enhances detrusor relaxation
    • Can be used for overactive bladder
  • Topical vaginal oestrogen can help improve bladder sensation and urgency in post-menopausal women
  • Duloxetine is occasionally used for incontinence
    • It is an SNRI
    • It increases sympathetic output to the urethral sphincter thereby increasing sphincter tone
    • Nausea if a common side-effect
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70
Q

What are the side effects of anticholinergic medications for incontinence?

A
  • Dry mouth
  • Constipation
  • Blurred vision
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71
Q

What is the surgical treatment for stress incontinence?

A
  • Surgery is a highly effective treatment option
    • Best surgical options:
      • Synthetic midurethral tape procedure
        • Cure rate for stress incontinence of 80-85%
        • This rate persists for 10+ years
        • Complications
          • Voiding difficulty (usually short term)
          • Bladder perforation during the procedure
          • Onset of new OAB symptoms after surgery
      • Burch colposuspension
        • Older procedure
        • Cure rate for stress incontinence of 80-85%
        • Similar complications
        • Added complication is a long-term risk of posterior vaginal prolapse
      • Periurethral injections to bulk up the bladder neck and coat the urethral mucosa (e.g. macroplastique)
        • Usually used for women deemed unfit for general anaesthesia
        • Lower cure rates than colposuspension and midurethral tape
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72
Q

What is the surgical management of detrusor overactivity?

A
  • Surgery may be second-line
  • Botulinum toxin is a highly effective treatment
  • It works by preventing release of neurotransmitter vesicles from the motor end-plate and causes flaccid paralysis in the muscle
  • It can be injected at multiple points within the bladder to abolish the involuntary detrusor contractions that cause symptoms
  • Achieves continence rates > 40%
  • Can lead to voiding difficulty
  • It does, nonetheless, provide a higher degree of social independence to patient
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73
Q

What are the symptoms of prolapse?

A
  • Sensation of vaginal bulge, heaviness or visible protrusion at or beyond the introitus
  • Lower abdominal/back pain
  • Dragging discomfort relieved by lying or sitting
  • Difficulty voiding urine
  • Difficulty emptying bowels
  • Sensation of incomplete emptying or bladder or rectum
    • NOTE: patients may need to support or reduce the prolapse with their fingers to be able to void or evacuate stool completely (referred to as digitation)
  • Urinary or faecal incontinence
  • Difficulty achieving penetration during sex
  • Pain/discomfort during sex
  • Loss of sensation or difficulty achieving orgasm due to vaginal or introital laxity
  • Vaginal bleeding (exclude endometrial cancer)
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74
Q

What are the risk factors for prolapse?

A
  • Childbirth

- Thinning of the puborectalis muscle

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75
Q

What is a uterovaginal prolapse caused by?

A
  • Uterovaginal prolapse is caused by failure of the interaction between the levator ani muscles and the ligaments and fascia that support the pelvic organs
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76
Q

What are the three levels of supporting ligaments and fascia that support the uterus, vagina and other organs?

A
  • Level 1 (Apical)
    • Uterosacral ligaments attach the cervix to the sacrum
    • This is important in supporting the vaginal walls
    • DEFECTS in level 1 can lead to descent of the uterus within the vagina
    • It is important to reattach the uterosacral ligaments during hysterectomy to prevent vaginal vault prolapse
  • Level 2
    • Provided by the fascia around the vagina (anterior, posterior, pubocervical (between the vagina and bladder) or rectovaginal (between vagina and rectum) fascia)
    • The fascial sheets fuse at the vaginal edge and are attached to the pelvic side wall (during with the obturator internus fascia)
    • The fascial attachments result in the vagina lying as a flattened tube at rest
    • DEFECTS in level 2 result in prolapse of the vaginal wall into the vaginal lumen (anterior or posterior vaginal prolapse)
    • The bladder or rectum will also prolapse behind the vaginal wall due to the fascial attachment
  • Level 3
    • Provided by the fascia of the posterior vagina (attached to the caudal end of the perineal body)
    • The perineal body is the mass of tissue that is torn or cut during childbirth
    • It is the point of attachment of the posterior vaginal fascia, fibres of levator ani and transverse perineal muscles
    • DEFECTS of the perineal body cause development of lower posterior vaginal wall prolapse
    • However, loss of the perineal body increases the size of the vaginal opening and predisposes to anterior vaginal prolapse as well
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77
Q

What should be asked in a history of prolapse?

A
  • Specific questions should be asked about sexual discomfort and difficulty achieving orgasm
  • If the woman is NOT sexually active, it should be explored whether this is because of anxieties or embarrassment of the appearance of the genitalia/loss of perceived attractiveness
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78
Q

How is a potential prolapse examined?

A
  • Lithotomy position with Sims speculum
  • Three Stages of Descent
    • Stage 1: prolapse does NOT reach the hymen
    • Stage 2: prolapse reaches the hymen
    • Stage 3: prolapse is mostly or wholly outside the hymen
      • NOTE: when the uterus prolapses wholly outside, it is called procidentia
  • A note should also be made about whether the prolapse occurs when the patient is straining or at rest and whether traction is applied
  • Assess whether the perineal body is intact or has been attenuated (resulting in enlarged vaginal opening)
  • If the woman has additional indirect symptoms (e.g. issues with bladder and bowel function) it would be appropriate to arrange urodynamic assessment or functional tests of the lower bowel (e.g. endoanal ultrasound to check for anal sphincter defects (rectal manometry, flexisig, defaecating proctogram)
  • An MDT approach is essential
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79
Q

What is a vaginal prolapse of the anterior vagina called?

A
  • Cystocele - if in the upper half of the vagina

- Urethrocele - if in the lower half of the vagina

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80
Q

What is a vaginal prolapse of the posterior vagina called?

A
  • Enterocele - if in the upper third of the vagina

- Rectocele - if in the lower two-thirds of the vagina

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81
Q

What is conservative treatment for prolapse?

A
  • Pelvic floor exercises (unlikely to be useful if prolapse is beyond the vaginal introitus)
  • Supportive vaginal pessaries
    • Ring pessaries are usually tried first
    • There is a range of options
    • Usually replaced every 6 months
    • Complications are uncommon
    • Sexual intercourse is theoretically possible with a well-placed ring pessary but not with others
    • Some patients can be taught to insert and remove their pessaries if they would like to remain sexually active
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82
Q

Describe surgery for pelvic organ prolapse

A
  • Principles for Prolapse Surgery
    • Remove/reduce the vaginal bulge
    • Restore the ligament/tissue supports to the apex, anterior and posterior vagina
    • Replace associated organs win their correct positions
    • Retain sufficient vaginal length and width to allow intercourse
    • Restore the perineal body
    • Correct or prevent urinary incontinence
    • Correct or prevent faecal incontinence
    • Correct obstructed defecation
  • Usually performed through the vagina to restore the ligamentous tissue support to the apex, anterior and posterior vagina and to repair the perineal body
  • The vaginal route can also be used for posthysterectomy vaginal vault prolapse to attach the vaginal vault to the right sacrospinous ligament
  • An abdominal approach to perform a sacrocolpopexy is also possible
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83
Q

What are the differential diagnoses of a pelvic mass? (Gynaecological)

A
  • Benign or malignant ovarian cyst
  • Ovarian torsion
  • Para-ovarian cyst
  • Ectopic pregnancy
  • Hydrosalpinx
  • Pyosalpinx
  • Tubo-ovarian abscess
  • Tubal malignancy
  • Pregnancy
  • Fibroids
  • Uterine malignancy
84
Q

What are the differential diagnoses of a pelvic mass? (Gastrointestinal)

A
  • Small or large bowel obstruction
  • Diverticular/appendicular abscess
  • Intussusception
  • Malignancy
85
Q

What are the differential diagnoses of a pelvic mass? (Urological)

A
  • Hydronephrosis
  • Pelvic kidney
  • Renal/bladder malignancy
86
Q

What are the other differential diagnoses of a pelvic mass? (Besides gynae, gastro and uro)

A
  • Pelvic lymphocele
  • Peritoneal cyst
  • Psoas muscle abscess
  • Lymphoma
  • Neuroblastoma
  • Aortic aneurysm
87
Q

Which demographics are function cysts, germ cell tumours and benign epithelial tumours more common in?

A
  • Functional cysts are common in young girls, adolescents and women in their reproductive years
  • Germ cell tumours occur more commonly in young women
  • Benign epithelial tumours are more common in older and post-menopausal women
  • Acute pain may represent torsion of a cyst or rupture/haemorrhage into it
88
Q

What is ovarian torsion?

A
  • Refers to rotation of the vascular pedicle supplying the ovary, which compresses and cuts its blood supply
  • This is more likely if the ovary is enlarged (e.g. when a cyst is present)
  • Up to 15% of dermoid cysts present acutely with torsion
89
Q

What are the presenting symptoms of ovarian torsion?

A
  • Acute onset lower abdominal pain

- Nausea and vomiting

90
Q

How is ovarian torsion diagnosed?

A
  • Pelvic USS with Doppler measurement of blood flow may be useful
  • Torsion of a normal ovary is VERY unlikely
91
Q

What is the management of ovarian torsion?

A
  • Untwist the ovary and its attached pedicle
  • Removal of the ovarian cyst
  • If surgery is not prompt enough, removal of a necrotic ovary may be necessary
  • Decision to operate should be based on clinical findings with TVUSS support
92
Q

How is ovarian torsion investigated?

A
  • 1st line for women with a suspected pelvic mass or pelvic pain = USS
    • Transvaginal - better resolution
    • Transabdominal - recommended in women who have never been sexually active
  • CT and MRI can further characterise the ovarian cyst
  • Pregnancy test - exclude pregnancy
  • Inflammatory markers - if appendicitis or tubo-ovarian abscess are differentials
93
Q

What are functional ovarian cysts?

A
  • Includes:
    • Follicular cysts
    • Corpus luteal cysts
    • Theca luteal cysts
  • Risk of functional ovarian cysts is REDUCED by the COCP
  • Diagnosis is made when the cyst measures > 3 cm (normal ovulatory follicles may reach 2.5 cm)
  • Tend to appear as simple unilocular cysts on USS
94
Q

What is the management of asymptomatic functional ovarian cysts?

A
  • Reassurance and repeat USS to check resolution or non-enlargement before discharge
95
Q

What is the management of symptomatic functional ovarian cysts?

A
  • Laparoscopic cystectomy
96
Q

What are corpus luteal cysts?

A
  • Cysts that occur following ovulation

- May present with PAIN due to rupture or haemorrhage (usually late in the menstrual cycle)

97
Q

What is the management of corpus luteal cysts?

A
  • Expectant (with analgesia)
  • Occasionally, surgery is necessary if there has been significant bleeding to wash out the pelvis and perform an ovarian cystectomy
98
Q

What are theca luteal cysts?

A
  • Cysts associated with pregnancy (especially multiple pregnancy)
  • Often bilateral
  • May be diagnosed incidentally on ultrasound
  • Usually resolve spontaneously during pregnancy
99
Q

What are inflammatory ovarian cysts?

A
  • Cysts ssually associated with pelvic inflammatory disease (PID)
  • Can involve the tubes, ovaries and bowel
  • Inflammatory markers are an important part of the investigations
  • Patients may have endometriomas
    • Sometimes referred to as ‘chocolate cysts’ due to the presence of altered blood within the ovary
    • Characteristic ground glass appearance on USS
100
Q

What is the treatment of inflammatory ovarian cysts?

A
  • Antibiotics
  • Surgical drainage
  • Surgical excision
    • NOTE: definitive surgery is usually deferred until after the acute infection has resolved
101
Q

What are germ cell tumours?

A
  • MOST COMMON ovarian tumours in young women (20-40 years)
  • Most common form of benign germ cell tumour: mature dermoid cyst (cystic teratoma)
    • Contains fully differentiated tissue types from all three germ cell layers
    • Up to 10% are bilateral
    • Low risk of malignant transformation
  • Usually diagnosed with pelvic USS
  • MRI may be useful
102
Q

What is the management of germ cell tumours?

A
  • Usually ovarian cystectomy is needed (spontaneous resolution is unlikely)
  • Surgery is particularly necessary if:
    • Symptomatic
    • 5+ cm diameter
    • Enlarging
  • Surgery prevents torsion and allows histological analysis
103
Q

What are epithelial tumours?

A
  • Benign epithelial tumours increase in frequency with age
  • MOST COMMON in perimenopausal women
  • Most common type: serous cystadenoma
    • Usually unilocular and unilateral
  • Mucinous cystadenomas are large, multiloculated cysts that are bilateral in 10% of cases
  • Brenner tumours are small tumours usually found incidentally in the ovary
    • Contain urothelial-like epithelium
    • Rarely secretes oestrogen
104
Q

What are sex cord stromal tumours?

A
  • MOST COMMON type: ovarian fibromas
    • Solid ovarian tumours composed of stromal cells
  • Tend to occur in older women
  • Usually presents with torsion
  • May, occasionally, present with Meig syndrome (pleural effusion, ascites and ovarian fibroma)
  • The pleural effusion usually resolves after removal of the ovarian fibroma
105
Q

What are thecomas?

A
  • Benign oestrogen-secreting tumours
  • Often present after menopause
  • Can cause features of excess oestrogen (e.g. postmenopausal bleeding)
  • Can induce an endometrial carcinoma
106
Q

What are some other ovarian cysts?

A
  • Fimbrial cyst
  • Paratubal cyst
  • Paraovarian cysts of Morgani
107
Q

What is endometriosis?

A
  • Endometrial tissue lying outside the uterine cavity
  • Usually found in the pelvic
  • Commonly located on the peritoneum lining the pelvic side walls, pouch of Douglas, uterosacral ligaments and bladder
  • When endometrial tissue is implanted into the ovary, an endometrioma forms
    • This may contain old, altered blood giving it a chocolate cyst appearance
  • Rarely, endometriosis an be found in the umbilicus, abdominal scars and pleural cavity
  • Endometriotic tissue responds to hormonal changes
  • Repeated episodes of bleeding and healing lead to fibrosis and adhesion formation between pelvic organs, leading to pain and infertility
  • Adenomyosis is often seen with endometriosis
    • Islands of endometrial tissue are found deep within the myometrium
108
Q

What is the incidence of endometriosis?

A
  • 5-10% of women of reproductive age
  • Found in 1/3 of women undergoing diagnostic laparoscopy for pelvic pain or infertility
  • It is oestrogen-dependent so it resolves after menopause or when treatment induces a pseudomenopause
109
Q

What is the aetiology of endometriosis?

A
  • Sampson’s Implantation Theory
    • Retrograde menstrual regurgitation of viable endometrial glands along patent Fallopian tubes and subsequent implantation on the pelvic peritoneal surface causes endometriosis
  • Meyer’s Coelomic Metaplasia Theory
    • Coelomic epithelium transformation refers to the de-differentiation of peritoneal cells linng the Mullerian duct back to their primitive origin (which then become endometrial cells)
  • Some genetic and ethnic influences (more common in oriental women, less common in Afro-Caribbean women)
  • Rarely, endometrial tissue can embolise through the vascular and lymphatic system and deposit in distant sites (e.g. pleural cavity)
110
Q

What are general clinical features of endometriosis?

A
  • Severe cyclical non-colicky pelvic pain
  • Occurs around the time of menstruation (may occur a few days before menses starts until the end of menses)
  • May be associated with heavy menstrual loss
  • Severe fatigue
  • NOTE: there is a lack of correlation between the extent of disease and the intensity of symptoms
  • Deep dyspareunia and pain on defecation (dyschezia) are key indicators of the presence of endometriosis deep within the pouch of Douglas
  • Endometriosis at distant sites can cause bizarre symptoms (e.g. cyclical epistaxis, cyclical rectal bleeding)
111
Q

What are symptoms of endometriosis? (Female Reproductive Tract)

A
  • Dysmenorrhoea
  • Lower abdominal and pelvic pain
  • Dyspareunia
  • Rupture/torsion of endometrioma
  • Low back pain
  • Infertility
112
Q

What are symptoms of endometriosis? (Urinary Tract)

A
  • Cyclical haematuria/dysuria

- Loin/flank pain (ureteric obstruction)

113
Q

What are symptoms of endometriosis? (GI Tract)

A
  • Dyschezia (pain on defecation)
  • Cyclical rectal bleeding
  • Obstruction
114
Q

What are symptoms of endometriosis? (Surgical Scars/Umbilicus)

A
  • Cyclical pain, swelling and bleeding
115
Q

What are symptoms of endometriosis? (Lung)

A
  • Cyclical haemoptysis

- Haemopneumothorax

116
Q

How is endometriosis diagnosed?

A
  • Physical Examination
  • Ultrasound
  • MRI
  • Laparoscopy
  • Biomarkers
117
Q

What is seen in the physical examination of endometriosis?

A
  • A normal vaginal examination does NOT rule out endometriosis
  • Findings suggestive of endometriosis:
    • Thickening or nodularity of the uterosacral ligaments
    • Tenderness in the pouch of Douglas
    • Adnexal mass
    • Fixed retroverted uterus
118
Q

What is seen on ultrasound and MRI for endometriosis?

A

Ultrasound
- TVUSS can diagnose endometriosis involving the ovaries (e.g. endometriomas)

  • It is less useful for diagnosing smaller lesions
  • TVUSS may be useful for rectal disease
  • Negative scans do NOT exclude endometriosis

MRI
- Can detect lesions > 5 mm

119
Q

What is seen on laparoscopy for endometriosis?

A
  • Traditional method of diagnosis
  • Based on the accuracy of visual diagnosis of endometriotic lesions (experience-dependent)
  • Appearances of endometriotic lesions:
    • Red
    • Puckered, black matchstick
    • White fibrous
  • Laparoscopy allows lesions to be biopsied for histological confirmation
  • Allows concurrent surgical diathermy and /or excision and staging of the disease
  • Patency of the Fallopian tubes can also be assessed
120
Q

What biomarkers are used for endometriosis?

A
  • CA125 has been explored as a biomarker for endometriosis

- Currently too inaccurate for clinical use

121
Q

How does endometriosis affect fertility?

A
  • 30-40% of patients with endometriosis complain of difficulty conceiving
  • It is not fully understood why endometriosis can lead to subfertility
  • Medical treatment of endometriosis does NOT improve fertility and should NOT be given to patients wishing to conceive
  • On the other hand, surgical ablation/excision of minimal and mild endometriosis does improve fertility
  • It is uncertain whether surgical treatment of endometriomas increases pregnancy rates (because it may damage ovarian tissue)
  • Currently thought that endometriomas should be left alone prior to IVF unless they are symptomatic or reduce access for egg collection
122
Q

What are some principles for endometriosis management?

A
  • Analgesics and hormonal ovarian suppression can be effective for treating pelvic pain associated with endometriosis
  • Medical treatment of presumed endometriosis can be started if the clinical examination/TVUSS are normal without the need for invasive laparoscopy
    • If no symptom relief is achieved after 3-6 months, a laparoscopy should be considered
  • Co-existing additional diseases such as IBS and constipation (seen in up to 80% of cases) should also be treated
  • Endometriosis is known to recur throughout reproductive life so it is impossible to guarantee complete cure
  • Treatment should be based on the age, symptoms, extent of disease and desire to have children
123
Q

What is medical therapy for endometriosis?

A
  • Analgesics
    • NSAIDs are useful for reducing severity of dysmenorrhoea and pelvic pain
    • Codeine/opiates should be AVOIDED because it could worsen co-existing IBS
  • Combined OCP
    • If pregnancy and contra-indications are absent, the COCP should be considered
    • It reduces endometriosis-associated dyspareunia, dysmenorrhoea and non-menstrual pain
    • It also provides cycle control and contraception
    • It can be taken for 21 days with a 7 day pill-free break but it may be more effective at alleviating symptoms if tricycled (3 packets taken back to back)
    • It can also be taken without a break to induce amenorrhoea
    • If this achieves symptomatic relief, it can be continued for several years until pregnancy is intended
    • If ineffective, consider treatment for co-existing conditions (e.g. IBS) and changing the medical management
  • Progestogens
    • Used to induce amenorrhoea in those with contraindications for the COCP
    • The depot-medroxyprogesterone acetate and levonorgestrel IUS are particularly effective for providing long-term therapeutic effect (particularly after surgery)
  • GnRH Agonists
    • Effective at relieving the severity and symptoms of endometriosis
    • Usually administered as slow-release depot formulations (lasting 1 month or more)
    • It should NOT be used for > 6 months because of the risk of osteoporosis
    • Also available as multiple, daily-administered intranasal sprays
  • Other hormonal agents
    • Ovarian suppressive agents (e.g. danazol, gestrinone) are no longer used
    • Current research is exploring aromatase inhibitors for endometriosis
124
Q

Describe surgical treatment for endometriosis

A
  • Fertility Sparing Surgery
    • Most operations can be achieved laparoscopically
    • Endometriotic chocolate cysts should have their inner cyst lining excised to reduce recurrence
      • However, this could result in damage to ovarian tissue
      • So, if the patient is also receiving fertility treatment, only drainage should be considered
    • Deposits of superficial peritoneal endometriosis can be easily ablated or excised during laparoscopy using diathermy or laser energy
    • Specialist surgery may be needed if the endometriosis has caused extensive adhesions or involved other organs
    • Risk of recurrence following surgery is as high as 30% so long-term medical therapy is often necessary and started straight after surgery
  • Hysterectomy and Oophrectomy
    • Hysterectomy with removal of the ovaries and all visible endometriosis lesions should be considered in women who have completed their family and failed to respond to conservative treatments
    • The woman should be informed that hysterectomy will NOT necessarily cure the symptoms or the disease
    • Oestrogen-only HRT can be started immediately after surgery once the patient is mobile
    • Some surgeons may prefer deferring HRT until about 6 months after surgery to prevent activation of any residual disease
    • Combined HRT can also be used if reactivation of new or residual disease is suspected
125
Q

What is chronic pelvic pain?

A
  • Intermittent or constant pain in the lower abdomen or pelvis of a woman of at least 6 months duration, NOT occurring exclusively with menstruation (dysmenorrhoea) or intercourse (dyspareunia) and not associated with pregnancy
126
Q

What is the incidence of chronic pelvic pain?

A
  • 20% of all outpatient appointments in gynaecological secondary care
  • Very COMMON
  • Prevalence of 10-20%
127
Q

What is aetiology of chronic pelvic pain?

A
  • Gynaecological
    • Endometriosis and adenomyosis
    • Adhesions including chronic PID
    • Uterine fibroids
    • Ovarian cysts
  • Central and Peripheral Nervous System
    • Modified pain perception (e.g. visceral hyperalgesia and neuropathic pain)
  • Gastrointestinal
    • IBS
    • Constipation
    • IBD
    • Coeliac disease
  • Urological
    • Bladder pain syndrome (pain, pressure or discomfort related to the bladder along with at least one other urinary symptoms (e.g. urgency or frequency) in the absence of other pathology)
    • Recurrent UTI
    • Urinary tract calculi
  • Musculoskeletal
    • Degenerative joint disease
    • Spondylolisthesis
  • Nerve Entrapment
  • Psychological and Social Issues
    • Depression, anxiety and sleep disorders
    • Physical and sexual abuse
128
Q

What are the investigations for chronic pelvic pain?

A
  • History should explore:
    • Pattern or pain
    • Association with other problems (e.g. psychological, bladder and bowel)
    • Effect of movement and posture
  • Examination: abdominal and pelvic to look for areas of tenderness or masses
  • Genital Tract Swab
    • All sexually active women should be offered screening for STIs
    • PID can cause chronic pelvic pain
  • Pelvic USS
    • Conducted if pelvic mass is suspected
    • Potential diagnoses include ovarian cysts, endometriomas, hydrosalpinges, tubo-ovarian abscess or uterine pathology (adenomyosis, fibroids)
  • MRI
    • Conducted if further assessment of pelvic masses is needed or there is suspected deep infiltrating endometriosis
  • Laparoscopy (GOLD standard but most invasive)
    • If pelvic masses, endometriosis or adhesions are suspected
    • Potential diagnoses include superficial/deep infiltrating endometriosis, abdominopelvic adhesions and pelvic masses
129
Q

What is the management of chronic pelvic pain?

A
  • General health advice is important (diet, hydration, exercise and sexual health)
  • Analgesia (NSAIDs, opiates and paracetamol)
  • If clinical examination and USS are normal in a woman with cyclical CPP, a therapeutic trial of hormonal treatment to suppress ovarian function for 3-6 months should be conducted before diagnostic laparoscopy
  • Hormonal treatments
    • COCP
    • LNG-IUS
    • Systemic progestogens
    • GnRH analogues
  • Structural pathology can be treated surgically (e.g. removal of adnexal masses)
  • Referral to relevant specialist if the cause of CPP is thought to be non-gynaecological
  • If pain persists, referral to a pain management team may be considered
130
Q

Describe the Uterine cervix

A
  • The cervix is the cylindrical lower extremity of the uterus
  • Consists mainly of collagen fibres
  • The vaginal part of the cervix (ectocervix) is lined by thick non-keratinised stratified squamous epithelium and has a pink appearance
  • The external os is visible in the centre of the ectocervix as a dark circular or slit-like area
  • It is the opening to the endocervical canal
  • The endocervical canal is lined by simple columnar epithelium
  • The point at which the simple columnar epithelium of the endocervical canal changes to the stratified squamous epithelium of the ectocervix is called the squamocolumnar junction
131
Q

What is cervical ectropion?

A
  • Cervical ectropion is a condition in women of reproductive age, where the columnar epithelium is visible on the ectocervix as a round, red area surrounding the external cervical os (this is NORMAL)
  • Ectropion normally develops under the influence of the THREE Ps:
    • Puberty
    • Pill
    • Pregnancy
  • A large cervical ectropion may be fragile leading to intermenstrual and postcoital bleeding
  • Some women may complain of an excessive, clear, odourless mucus-type discharge
132
Q

What is the management of cervical ectropion?

A
  • Changing from oestrogen-based hormonal contraceptives can reduce symptoms
  • Cervical ablation (cryocautery done as an outpatient)
  • Cervical and lower genital tract swabs should be taken to exclude STI
  • A smear should also be taken to exclude cervical premalignancy/malignancy
133
Q

What are nabothian follicles?

A
  • When the columnar glands within the transformation zone become sealed over, forming small, mucous-filled cysts visible on the ectocervix
  • They have NO pathological significance
  • NO treatment is required
  • Very large ones may need drainage
134
Q

What are cervical polyps?

A
  • Benign tumours arising from the endocervical epithelium
  • May be seen as smooth, reddish protrusions
  • Usually asymptomatic
  • May be detected incidentally on routine cervical smear
  • Can cause vaginal discharge, IMB and PCB
  • Easily removed by avulsion with polyp forceps as an outpatient
135
Q

What is cervical stenosis?

A
  • Pathological narrowing of the endocervical canal
  • Usually iatrogenic (caused by surgery)
    • E.g. cone biopsy, loop diathermy and endometrial ablation
  • Entrapment of blood within the uterus (haematometra) causes cyclical dysmenorrhoea with no associated menstrual bleeding
136
Q

What is the management of cervical stenosis?

A
  • Surgical dilatation of the cervix under ultrasound or hysteroscopic guidance
137
Q

What are endometrial polyps?

A
  • Focal endometrial outgrowths containing a variable amount of glands, stroma and blood vessels (so have a varying appearance)
  • May be asymptomatic
  • Can cause abnormal uterine bleeding (HMB, IMB and PMB)
  • Can adversely impact fertility
  • COMMON - seen in 10-20% of women with AUB and 10% of women with subfertility
  • Polyps tend to be insensitive to cyclical hormonal changes (so can cause unscheduled vaginal bleeding)
  • 10-25% of symptomatic endometrial polyps contain hyperplastic foci and 1% are malignant
  • Endometrial polyps may be
    • Pedunculated or sessile
    • Single or multiple
    • Vary in size (0.5-4 cm)
138
Q

What are the risk factors of endometrial polyps?

A
  • Obesity
  • Late menopause
  • Tamoxifen
  • HRT
139
Q

What investigations are done for endometrial polyps?

A
  • TVUSS
  • Outpatient hysteroscopy (OPH) and saline infusion sonography (SIS) are the most accurate
    • These tests involve distending the uterine cavity
140
Q

What is the management of endometrial polyps?

A
  • Some small polyps may resolve spontaneously
  • Polypectomy recommended to alleviate AUB symptoms, optimise fertility and exclude hyperplasia/cancer
    • Can be performed as a day-case under general anaesthesia
    • Can also be performed as an outpatient with or without local anaesthesia
    • A hysteroscope is used to visualise the polyp and small instruments are used to remove the polyp
141
Q

What is Asherman’s syndrome?

A
  • Fibrosis and adhesion formation within the endometrial cavity following irreversible damage of the single layer thick basal endometrium (does not allow normal regeneration or the endometrium)
  • This results in:
    • Reduced/absent menstrual shedding
    • Subfertility
  • Conservative and less traumatic surgical approaches to managing retained products of conception
142
Q

What are the causes of Asherman’s syndrome?

A
  • Surgical breakdown of intrauterine adhesions (adhesiolysis)
  • NOTE: this risks further uterine trauma
143
Q

What are fibroids?

A
  • Benign tumour of the uterine smooth muscle (leiomyoma)
  • Macroscopically looks like a well-demarcated, firm, whorled tumour
  • Found in 40% of women
    • More common in nulliparous, obese and African women
  • Often multiple, and can considerably increase the size of the uterus
144
Q

How are fibroids classified?

A
  • Based on location relative to uterine wall
    • Submucous
    • Cervical
    • Intramural
    • Subserosal
  • Rarely, they can arise outside the uterus (e.g. broad ligament)
145
Q

What are the symptoms of fibroids?

A
  • Most are small and asymptomatic
  • Heavy menstrual bleeding and intermenstrual bleeding
  • Reproductive failure
  • Subfertility
  • Recurrent pregnancy loss
  • Bulk effects on adjacent structures in the pelvis
  • Pressure and pain
  • Bladder and bowel dysfunction
  • Abdominal distension
146
Q

What is the natural history of fibroids?

A
  • Fibroids are oestrogen-dependent so they can enlarge during pregnancy (due to hyper-oestrogenic state)
  • They tend to shrink after menopause
  • THREE forms of degeneration (due to outgrowing its blood supply) of a fibroid:
    • Red
      • Haemorrhage and necrosis occurs within the fibroid typically presenting in the mid-second trimester pregnancy with acute pain
    • Hyaline
      • Asymptomatic softening and liquefaction of the fibroid
    • Cystic
      • Asymptomatic central necrosis leaving cystic spaces at the centre
      • Degenerative changes can initiate calcium deposition leading to calcification
      • Very rarely, malignant or sarcomatous degeneration can occur
      • Suspicion is greatest in the postmenopausal period when there is rapidly increasing size of the fibroid
147
Q

What are the clinical features of fibroids?

A
  • VAST MAJORITY are asymptomatic
  • Examination Findings
    • General: signs of anaemia
    • Abdominal: visible and/or palpable abdominal mass arising from the pelvis
    • Bimanual: enlarged, firm, smooth or irregular non-tender uterus
  • Menstrual disturbance
  • Pressure/bulk symptoms
    • Urinary frequency
    • Infertility
  • Pain is UNUSUAL except for
    • Red degeneration
    • Torsion of pedunculated fibroid
148
Q

How do fibroids relate to Subfertility?

A
  • May result from mechanical distortion or occlusion of the Fallopian tubes
  • An endometrial cavity that is distorted by submucous fibroids may prevent implantation
    • Removal of submucosal fibroids can enhance fertility and improve outcomes for assisted reproductive techniques
  • Removal of other types of fibroids risks hysterectomy (1%) so surgical removal should be carefully considered
  • Risk of miscarriage is NOT increased once pregnancy is established
  • In late pregnancy, fibroids could cause an abnormal lie
  • After delivery, PPH may occur due to inefficient uterine contraction
149
Q

What investigations are done for fibroids?

A
  • Often a clinical diagnosis
  • FBC - check for anaemia
  • Ultrasound (MAINSTAY)
    • TVUSS
      • Good for detecting submucous fibroids and small intramural fibroids
    • TAUSS
      • Good for detecting larger intramural and subserosal fibroids and excluding hydronephrosis secondary to pressure from fibroids on ureters
    • Saline Infusion Sonography (SIS)
      • Good for detecting and locating submucosal fibroids and endometrial polyps
  • MRI may be used to demarcate morphology, size and location of fibroids
    • Useful for monitoring treatment response
    • Should be performed before uterine artery embolisation
  • Hysteroscopy
    • Good for detecting submucosal fibroids and endometrial polyps
    • Good for planning subsequent hysteroscopic surgical treatment
    • Surgical hysteroscopy can remove polyps, adhesions and submucosal fibroids
150
Q

How is the management of fibroids split up into?

A
  • Medical Treatment
  • Surgical Treatment
  • Radiological Treatment
151
Q

What is the medical management of fibroids?

A
  • Conservative management if asymptomatic fibroids
  • Main treatments for HMB
    • LNG-IUS
    • Tranexamic acid
    • Mefenamic acid
    • COCP
    • May be ineffective in the presence of submucous fibroid or an enlarged uterus that is palpable abdominally
  • Injectable GnRH Agonist
    • Only effective medical treatment
    • Induces a menopausal state (shuts down ovarian oestradiol production)
    • Poorly tolerated because of severe menopausal symptoms
  • Ulipristal Acetate (selective progesterone receptor modulator)
    • As effective as GnRH agonists in reducing fibroid volume and alleviating HMB symptoms
    • Not yet widely accepted into clinical practice
    • Does NOT induce a menopausal state
    • Can be taken orally
  • NOTE: neither of the above options are long-term - fibroids regrow as soon as ovarian function returns
152
Q

What is the surgical management of fibroids?

A
  • Depends on presenting complains and patient’s preferences regarding menstrual function and fertility
  • Minimally invasive hysteroscopic surgery can be used to remove submucous fibroids and fibroid polyps (which relieved HMB symptoms)
  • If the patient has a bulky fibroid uterus causing pressure symptoms or where HMB is refractory to medical interventions, there are THREE options:
    • Myomectomy
      • Preferred if preservation of fertility is required
      • Can be done laparoscopically (power morcellation is used to shrink the fibroids for removal)
      • There is a small but significant risk of uncontrolled life-threatening bleeding during myomectomy which may require a hysterectomy
    • Surgical removal of fibroids with uterine conservation
    • Hysterectomy
  • Hysterectomy and myomectomy could be preceded by GnRH agonist pre-treatment for 3 months to reduce the bulk and vascularity of the fibroids
    • This can facilitate a suprapubic incision and vaginal hysterectomy rather than midline abdominal incision and abdominal hysterectomy
    • This is associated with quicker recovery and fewer complications
153
Q

What is the radiological management of fibroids?

A
  • Uterine artery embolisation
    • Involves embolisation of both uterine arteries under radiological guidance
    • A cannula is passed through the femoral artery into the uterine artery
    • Embolisation induces infarction and degeneration of fibroids leading to a reduction in fibroid volume of around 50%
    • Patients usually require admission to deal with the pain associated with uterine artery occlusion (opiate analgesia)
    • Complications: fever, infection, fibroid expulsion, potential ovarian failure
    • Adequate counselling is important because the effect on reproductive function are uncertain
    • 1/3 of women require further medical, radiological or surgical treatment within 5 years
    • As effective as myomectomy for alleviating fibroid-related HMB and pressure symptoms
154
Q

What is adenomyosis?

A
  • Disorder in which endometrial glands and stroma are found deep within the myometrium
  • It can only definitively be diagnosed following histopathological examination of a hysterectomy specimen
  • The ectopic endometrium responds to cyclical hormonal changes resulting in bleeding within the myometrium
  • This manifests as:
    • Increasingly severe secondary dysmenorrhoea (pain through menses)
    • Uterine enlargement
    • HMB
  • Women are usually multiparous and diagnosed in their late 30s/early 40s
155
Q

What are the investigations for adenomyosis?

A
  • Examination: bulky and sometimes tender ‘boggy’ uterus
  • Ultrasound may show haemorrhage-filled, distended endometrial glands
    • May show an irregular nodular development (similar to fibroids)
  • MRI: BEST INVESTIGATION
    • Provides excellent resolution images
156
Q

What is the management of adenomyosis?

A
  • Any treatment that induces amenorrhoea will render the ectopic endometrium quiescent (thereby relieving pain and excessive bleeding)
  • So, use of progestin-containing long-acting reversible contraceptives (LARCs) should be considered
    • E.g. LNG-IUS, DepoProvero, short-term GnRH agonists
  • HOWEVER, symptoms return rapidly on ceasing treatment
  • Hysterectomy is the only definitive treatment
157
Q

What are the differential diagnosis of vulva complaints?

A
  • Vulval Pruritis
    • Infections (e.g. candidiasis, TV)
    • Skin conditions (e.g. lichen sclerosis, eczema, VIN)
    • Contact dermatitis
  • Vulval Pain
    • Infections (e.g. candidiasis)
    • Skin conditions (e.g. lichen sclerosis, eczema, VIN)
    • Vulvodynia (chronic vulval pain with no identifiable cause)
    • Bartholin gland infection
  • Superficial Dyspareunia
    • Skin conditions (e.g. lichen sclerosis leading to vulval splitting)
    • Vulvodynia
    • Vulval fissures
    • Skin bridges of the vulva
158
Q

How do you assess vulval conditions?

A
  • Full history and examination (potentially with vaginal swabs/biopsies)
  • Ask about general skin problems (general skin disorders like eczema and psoriasis can affect the vulva)
  • Discuss current methods of skin care (e.g. scented products can worsen symptoms)
  • Impact of symptoms on sexual functioning
159
Q

What are the most common presenting symptoms of vulval itching and discomfort?

A
  • Itching
  • Discomfort
  • Pain
  • Discharge
  • Dyspareunia
  • Affect all ages, in particular, postmenopausal women
  • Support group: Vulval Pain Society
  • Itching can lead to nocturnal involuntary itching
  • This can lead to dysuria as the urine burns the excoriated vulval skin
160
Q

How is reduction in allergens useful in vulva conditions?

A
  • Vulval dermatitis is strongly associated with a history of atopy
  • Therefore, allergen exposure should be reduced in all patients presenting with symptoms of vulval pruritus
  • Discourage women from washing with soaps or detergents that disrupt the bacterial balance of the vagina (water is a better alternative)
  • Encourage cotton underwear and washing clothing with an unperfumed washing powder/fabric conditioner
  • Sanitary pads may cause vulval dermatitis (so changing to unbleached, organic pads (moon cup))
161
Q

Describe recurrent use of antifungals and vulva pruritus

A
  • Some women will regularly be prescribed or receive OTC antifungals (e.g. clotrimazole cream and pessaries)
  • It may soothe initial symptoms but can cause a hypersensitivity reaction that worsens symptoms
  • Vulval and vaginal candidiasis is COMMON in women of reproductive age
  • It is uncommon in prepubescent and postmenopausal women
    • These women, therefore, should be checked for other causes of itching
    • Diabetes should be considered as a cause of recurrent thrush
  • Candidal infection should be treated with:
    • 150 mg clotrimazole nightly over 3 consecutive nights
    • 2nd line: oral fluconazole
  • NOTE: in menstruating women, thrush is more common postmenstrually due to changes in vaginal pH
  • There is no need to treat partners unless they are symptomatic
162
Q

How does ferritin affect vulva pruritus?

A
  • 5% of women with vulval pruritus have low ferritin

- Correction of this will improve symptoms

163
Q

Describe biopsy in vulva disease

A
  • Should only be performed if there is concern regarding MALIGNANCY
  • If diffuse leukoplakia or erythema treatment with steroids and emollients is recommended
    • If symptoms do NOT resolve, biopsy should be considered
  • Done by Keyes punch biopsy which can be done under local anaesthetic in clinic
  • Biopsies should also be carried out for pigmented lesions, raised or indurated areas and persistent ulcers
164
Q

What is Lichen Planus?

A
  • Autoimmune disorder affecting 1-2% of the population (particularly > 40 years) affecting the skin, genitalia and oral and GI mucosa
165
Q

What are the symptoms of lichen planus?

A
  • Pruritus
  • Superficial dyspareunia
  • Lesions in the mouth (reticular-like cobwebs)
    • Oral inspection is important
  • Longitudinal ridging of the nailbeds
  • Genital lesions
    • Longitudinal, annular, ulcerative, hyperpigmented or bullous
    • May cause vaginal stenosis and sexual dysfunction
166
Q

What is the management of lichen planus?

A
  • High-dose topical steroids

- If vaginal stenosis, dilatation with manual measures should be attempted in the first instance

167
Q

What is lichen sclerosus?

A
  • Destructive inflammatory skin condition that affects mainly the anogenital area of women.
  • Believed to be autoimmune (many patients have other autoimmune conditions (e.g. thyroid disease and pernicious anaemia))
  • Results in hyalinisation of the skin
  • Leads to fragility and white parchment paper appearance of the skin and loss of vulval anatomy
  • Associated with vulval cancer
168
Q

What are the symptoms of lichen sclerosus?

A
  • Itching
  • Soreness (usually due to scratching)
  • Hypopigmentation
  • Loss of anatomy
  • Vaginal stenosis and cracking (particularly at posterior fourchette)
169
Q

What is the management of lichen sclerosus?

A
  • Good skin care
  • Strong steroid ointments (e.g. clobetasol proprionate for 3 months)
  • Biopsy is indicated if the condition does not resolve with treatment
170
Q

What are vulval cysts?

A

Types

  • Bartholin’s cyst
  • Skene gland cyst
  • Mucous inclusion cyst
  • Can cause a lump with or without vulval discomfort
  • Bartholin’s cysts can become infected causing a Bartholin’s abscess
    • These usually present acutely
    • May require incision and drainage
      • Outpatient drainage is possible
      • May be accompanied by insertion of a tiny catheter to maintain patency for several weeks
  • May be managed by marsupialisation of the cyst
    • Involves suturing the internal aspect of the cyst to the outside of the cyst to prevent the cyst from reforming
    • Usually done under general or spinal anaesthesia
171
Q

What is vulvodynia?

A
  • A condition of pain of the vulva often described as a burning pain, occurring in the absence of skin disease of infection
  • It is a neuropathic pain syndrome
  • Classification
    • Anatomical site (generalised, localised or clitoral)
    • Provoked or unprovoked
  • Can occur at any age
  • Support: Vulval Pain Society
  • Neuromodulators (e.g. amitrytiline) can be useful in some women
  • Some may benefit from perineal massage
  • Oils may provide a barrier to precipitating factors (e.g. allergens, chafing)
  • Provide support to regain their sex lives
172
Q

What is dyspareunia?

A
  • Pain during or after sexual intercourse
    • Superficial: affecting the vagina, clitoris or labia
    • Deep: pain within the pelvis
  • Epidemiology
    • 10 - 20% prevalence
  • Risk Factors
    • FGM
    • Suspected PID
    • Endometriosis
    • Peri/postmenopausal
    • Depression and anxiety
    • History of sexual assault
173
Q

What should be asked in a history for dyspareunia?

A
  • Nature and onset of pain
  • Relationship to intercourse
  • Associated chronic pelvic pain symptoms
  • Reproductive and past medical history
  • Psychosexual history
174
Q

Describe the examination of dyspareunia

A
  • Nature and onset of pain
  • Relationship to intercourse
  • Associated chronic pelvic pain symptoms
  • Reproductive and past medical history
  • Psychosexual history
175
Q

How are superficial and deep dyspareunia investigated?

A
  • Superficial: consider biopsy of lower genital tract lesions or swabs
  • Deep: consider TVUSS, swabs and laparoscopy
176
Q

What is the treatment for dyspareunia?

A
  • Superficial: treat any identifiable cause

- Deep: treat as for chronic pelvic pain

177
Q

What is psychosexual dysfunction?

A
  • Primary: sexual difficulties where there may be psychosomatic pain
  • Secondary: sexual difficulties resulting from pain or emotional issues
178
Q

What is vaginismus and non-consummation?

A
  • DEFINITION: involuntary contraction of vaginal muscles during vaginal examination
  • Often leads to non-consummation and can cause considerable distress (fertility, relationship issues)
  • Traditionally, doctors and sex therapists used vaginal dilators to widen the opening but these rarely translate into sexual activity
  • There are various psychological influences (e.g. mentioning that you are using the ‘small speculum’ can reinforce the idea within the patient’s mind)
  • Encourage self-exploration at home with perineal massage and stretching of the vagina with fingers
  • Explore the patient’s anxieties and consider whether surgery is the best option
179
Q

What is FGM?

A
  • DEFINITION: any procedure involving partial or total removal of the external genitalia and/or injury to the female genital organs whether for cultural, religious or other non-therapeutic reasons
  • Can lead to physical, sexual and psychosexual issues
  • May even lead to renal failure due to urinary obstruction/infection
  • There is a legal obligation in the UK to document all cases and report all cases in minors through the safeguarding team
  • FGM in minors is considered child sexual abuse and social services and the police should be involved
  • There has been an increase in the number of patients requesting cosmetic surgery for their vaginas
  • Resource: The Great Wall of Vagina (hundreds of plaster casts of vulvas by a British artist)
180
Q

What are the four degrees of FGM?

A
  • Type 1: clitoroidectomy - excision of the clitoral hood with or without removal of the clitoris
  • Type 2: excision of the clitoris and partial or total removal of the labia minora
  • Type 3: excision of part of all of the external genitalia (clitoris, labia minora and majora) and stitching/narrowing the vagina (infibulation)
  • Type 4: piercing the clitoris, cauterisation, cutting the vagina, inserting corrosive substances. Also includes any plastic surgery procedures done as an adult
181
Q

What is de-infibulation?

A
  • Reversal of infibulation
  • Ideally should be identified pre-conceptually
  • Should be performed with adequate analgesia to avoid flashbacks of FGM
  • Incision is made along the vulval incision scar
  • Women should receive prior urinary infection screening and given appropriate antibiotics
  • Access to specialist services and support groups is necessary
182
Q

What is the classification of primary ovarian tumours?

A
  • Epithelial (80%)
    • High-grade serous
    • Endometrioid
    • Clear cell
    • Mucinous
    • Low-grade serous
  • Sex cord stromal
    • Granulosa cell
    • Sertoli-Leydig
    • Gynandroblastoma
  • Germ cell
    • Dysgerminoma
    • Endodermal sinus (yolk sac)
    • Teratoma
    • Choriocarcinoma
    • Mixed
183
Q

What are types of secondary ovarian tumours?

A
  • Secondary ovarian tumours (Krukenberg tumours) can come from
    • Colon
    • Stomach
    • Breast
184
Q

What are epithelial tumours?

A
  • Can be benign, malignant or borderline
  • 10% are classified as borderline ovarian tumours (BOTs) - well differentiated with some features of malignancy but do NOT invade the basement membrane
    • Most are serous tumours
    • BOTs can spread to other abdominopelvic structures but do not tend to recur following initial surgery
  • High-grade serous carcinoma accounts for 75% of all epithelial ovarian cancers
    • Mucinous and endometrioid account for 10%
    • Clear cell carcinoma is less common
    • High-grade serous is characterised by psammoma bodies (concentric rings of calcification)
  • Mucinous carcinomas are generally LARGE, multiloculated tumours associated with pseudomyxoma peritoneii
  • Endometrioid carcinomas have a similar histological appearance to endometrial cancer and are associated with endometriosis in 10% of cases and endometrial cancer in 10-15%
    • Associated with better survival
  • Clear cell carcinoma can also arise from endometriosis
185
Q

What are the aetiology and risk factors of high-grade pelvic serous carcinoma?

A
  • Often present with advanced disease so it is difficult to establish the anatomical site of origin
  • There may be a Fallopian tube precursor lesion called serous tubal intraepithelial carcinoma (STIC)
  • These are characterised by p53 mutations in the secretory cells of the distal Fallopian tube
  • 30% of high-grade pelvic serous cancers have BRCA mutations
186
Q

What are the aetiology and risk factors of Endometrioid, mucinous, clear cell, borderline and low-grade serous ovarian carcinomas?

A
  • Inclusion cysts of the ovarian surface epithelium and endometriosis can give rise to tumours
  • Endometriosis-associated ovarian cancers are usually endometrioid or clear cell
187
Q

What increases the risk of ovarian cancer?

A
  • Nulliparity
  • IUD
  • Endometriosis
  • Cigarette smoking (mucinous only)
  • Obesity
188
Q

What decreases the risk of ovarian cancer?

A
  • Multiparity
  • COCP
  • Tubal ligation
  • Salpingectomy
  • Hysterectomy
189
Q

Describe the genetic factors for ovarian cancer

A
  • 10-15% of women with ovarian cancer have a hereditary predisposition
  • Increased risk associated with:
    • BRCA1 and BRCA2
    • Lynch syndrome
  • Lifetime risk for general population = 1 in 70
  • Risk if 1 family member is affected = 1 in 20
  • BRCA accounts for 90% of hereditary cancers
    • BRCA 1 = 80%
    • BRCA 2 = 15%
  • Lynch syndrome is hereditary non-polyposis colorectal cancer (HNPCC) and is associated with endometrial cancer and a 10% lifetime risk of ovarian cancer
190
Q

What is the prevention for ovarian cancer?

A
  • Women who are positive for BRCA mutation are offered prophylactic bilateral salpingo-oophorectomy (BSO) when they have completed their families
  • This reduces the risk of ovarian cancer by 90%
  • Ovarian cancer tends to occur at a younger age in people with BRCA mutation (1 = 30s, 2 = 40s)
  • Bilateral salpingectomy with delayed oophorectomy may be a new, improved option based on the theory that BRCA-associated ovarian cancer originate in the Fallopian tube
    • Delayed oophorectomy offsets the morbidity associated with surgical menopause
  • Tubal ligation and hysterectomy can also reduce ovarian cancer risk
  • COCP reduces ovarian cancer risk by up to 50% in both BRCA mutation carriers and women at average risk of ovarian cancer
191
Q

What is the screening for ovarian cancer?

A
  • Screening with TVUSS and CA125 has not been shown to improve survival in women with a familial predisposition to ovarian cancer
  • This is because BRCA-associated ovarian cancers develop rapidly
192
Q

What are the clinical features for ovarian cancer?

A
  • Often non-specific and vague
  • MOST COMMON SYMPTOMS
    • Increased abdominal girth/bloating
    • Persistent pelvic pain and abdominal pain
    • Difficulty eating and feeling full quickly
  • Other symptoms
    • Change in bowel habit
    • Urinary symptoms
    • Back ache
    • Irregular bleeding
    • Fatigue
193
Q

What is seen on examination for ovarian cancer?

A
  • May reveal fixed, hard mass arising from the pelvis
  • Differential diagnosis for pelvic mass
    • Non-epithelial ovarian cancer
    • Tubo-ovarian abscess
    • Endometriomas
    • Fibroids
  • NOTE: ascites is highly suggestive of ovarian cancer
  • Chest examination for pleural fluid
  • Neck and groin should be examined for enlarged nodes
194
Q

How is ovarian cancer diagnosed?

A
  • TVUSS is the initial imaging modality of choice
  • Characterise in terms of:
    • Size
    • Consistency
    • Presence of solid elements
    • Bilaterality
    • Presence of ascites
    • Extraovarian disease (peritoneal thickening and omental deposits)
  • Tumour Markers
    • CA125 is also commonly raised in pregnancy, endometriosis and alcoholic liver disease
    • CA125 is raised in 80% of epithelial ovarian cancers
  • Risk of Malignant Index (RMI) can be calculated from menopausal status, pelvic ultrasound features and CA125 to triage pelvic masses
  • Pelvic pathology at intermediate or high risk malignancy should receive CT and/or MRI
    • CT is particularly useful for extrapelvic disease and staging
    • MRI helps determine operability
    • Other investigations: CXR, ECG, FBC, U&E, LFT
  • If there is gross ascites or pleural effusion, paracentesis or pleural aspiration may be required
  • Biopsy is needed before chemotherapy can be given (ultrasound or CT-guided)
195
Q

Describe FIGO staging

A
  • It can spread directly to the peritoneum and other organs
  • It can spread via the lymphatics to the pelvic and para-aortic nodes
196
Q

What is the surgical management of ovarian cancer?

A
  • Aims to stage the disease and remove all visible tumour
  • Most important prognostic factor is NO residual disease following laparotomy
  • Vertical incision is required to gain access
  • Total abdominal hysterectomy and BSO performed along with omentectomy
  • Ascites and peritoneal washings should be sampled
  • Further debulking may be required (e.g. resection of bowel, peritoneal stripping, splenectomy)
  • Lymph node resection is important
  • Young women with early-stage epithelial ovarian cancer may want fertility-sparing surgery
  • Fertility-sparing surgery may also be considered in patients with borderline tumours if fertility is an issue
  • If surgery is deemed unsuitable, chemotherapy may be offered
  • ‘Second look’ surgery is a planned laparotomy at the end of chemotherapy
  • This aims to assess for residual disease
  • After surgery, the MDT should discuss the need for chemotherapy
197
Q

How does chemotherapy treat ovarian cancer?

A
  • Can be given as primary treatment, an adjunct following surgery or for relapse of disease
  • 1st line: combination of a platinum compound with paclitaxel
  • Most are given as an outpatient, 3 weeks apart for 6 cycles
  • Platinum compounds
    • Most effective in ovarian cancer
    • Cause cross-linkage of DNA stands leading to cell cycle arrest
    • Carboplatin is the main platinum compound used as it is less nephrotoxic and causes less nausea than cisplatin
    • Does of carboplatin is calculated using the GFR
  • Paclitaxel
    • Causes microtubular damage
    • Prevents replication and cell division
    • Pre-emptive steroids are given to reduce hypersensitivity reactions and reduces side-effects (e.g. peripheral neuropathy, neutropaenia and myalgia)
    • Causes total loss of body hair
  • Bevacizumab
    • Monoclonal antibody against VEGF
    • Inhibits angiogenesis
    • Not routinely prescribed in ovarian cancer due to cost
    • Available for the treatment of recurrent disease
  • Patients will undergo a CT scan following completion of chemotherapy to assess response to treatment
  • Follow-up includes clinical examination and CA125 measurement
    • CA125 tends to rise prior to the onset of clinical evidence of disease recurrence
    • When disease recurs, treatment is largely palliative
198
Q

What is the prognosis of ovarian cancer?

A
  • Depends on stage, volume of disease following surgery and histological grade
  • 5-year survival = 46% (stage 1 = 90%; stage 3 = 30%
199
Q

What are primary peritoneal carcinomas?

A
  • High-grade serous carcinoma
  • Histologically same as tumours coming from the Fallopian tubes and ovaries
  • Criteria for Diagnosis:
    • Normal sized or slightly bulky ovaries
    • More extraovarian disease than ovarian disease
    • Low volume peritoneal disease
  • Natural history, prognosis and treatment are the same as for other high-grave pelvic carcinomas
200
Q

What are sex cord stromal tumours?

A
  • 10% of all ovarian tumours
  • Low malignant potential and good prognosis
  • Morbidity may arise from oestrogen-producing (granuloa, theca, Sertoli) and androgen-producing (Sertoli-Leydig, steroid cell)
  • This can result in precocious puberty, abnormal menstrual bleeding and an increased risk of endometrial cancer
  • Granulosa cell tumours are the most common type of sex cord stromal tumour
201
Q

What are the clinical features of sex cord stromal tumours?

A
  • Manifestations of hormone production
    • Irregular menstrual bleeding
    • Postemenopausal bleeding
    • Precocious puberty
  • Granulosa cell tumours may present with:
    • Large pelvic mass
    • Pain due to torsion/haemorrhage
    • May produce inhibin which can be used to follow-up surveillance
  • Sertoli-leydig cell tumours produce androgens and may present with:
    • Pelvic mass
    • Signs of virilisation (amenorrhoea, deep voice, hirsutism)
    • Can produce renin leading to hypertension
  • Most sex cord stromal tumours present as unilateral ovarian masses
202
Q

What is the management of sex cord stromal tumours?

A
  • Based on age and wish to preserve fertility
  • If YOUNG, unilateral salpingo-oophorectomy, endometrial sampling and staging is sufficient
  • In OLDER patients, full surgical staging is recommended
  • Granulosa cell tumours can recur after many years so requires long-term follow-up
  • Surgery is the mainstay of treatment (no effective chemotherapy)
203
Q

What are germ cell tumours?

A
  • Occur mainly in YOUNG women
  • Account for 10% of ovarian tumours
  • Dysgerminomas are 50% of germ cell tumours
    • Bilateral in 20%
    • Occasionally secrete hCG
  • Endodermal sinus yolk sac tumour is the SECOND most common (15%)
    • Secrete alpha-fetoprotein
    • Large solid mass
    • Often causes acute symptoms with torsion or rupture
    • Spreads late, usually to the lungs
  • Immature teratomas are 15-20% of malignant germ cell tumours
    • Mature or immature depending on the grade of neural tissue present
    • Occasionally there is malignant transformation of a cell type within the mature teratoma (usually squamous cell carcinoma)
  • Non-gestational choriocarcinoma is a VERY RARE type of tumour that usually occurs in young girls (irregular bleeding, high hCG)
204
Q

What are the presenting symptoms of germ cell tumours?

A
  • Pelvic mass
  • 10% present acutely with torsion or haemorrhage
  • 70% will be stage 1
205
Q

What are clinical features and investigations of germ cell tumours?

A
  • Young women presenting with a pelvic mass that is rapidly growing
  • Tumour markers
  • MRI to assess morphology
  • CT to check liver and lymph nodes
  • CXR for pulmonary metastases
206
Q

What is the management of germ cell tumours?

A
  • Fertility-sparing treatment may be preferred (because most women are of reproductive age)
  • Exploratory laparotomy to remove the tumour and assess contralateral spread to other ovary
  • Careful inspection of the abdominal cavity is required with peritoneal biopsies and sampling of any enlarged pelvic or para-aortic nodes
  • Postoperative chemotherapy depends on stage
    • Most common regime = bleomycin, etoposide and cisplatin (BEP)
    • Given as 3-4 treatments 3 weeks apart
    • 90% cure rates
  • If recurrence, 90% will present within the first year of diagnosis and salvage chemotherapy has good success rates