Specialist Gynae Flashcards

1
Q

What is Urinary incontinence?

A

Involuntary leakage of urine that is objectively demonstrable and sufficient enough to cause physical and/ or emotional distress.

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2
Q

What is the physiology of urinating?

A
  • Detrusor muscle makes up bladder wall
  • Parasympathetic nerves aid voiding. Sympathetic nerves prevent voiding
  • Micturition reflex controlled at the pons
  • Afferent fibres respond to distension of the bladder wall at spinal cord
  • Efferent parasympathetic fibres = contraction of detrusor muscle and opening of bladder neck
  • Sympathetic fibres inhibit this
  • Cerebral cortex modifies reflex and can relax or contract striated muscle of urethra and pelvic floor
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3
Q

What are the causes of Urinary incontinence?

A

• Reduced intra-urethral pressure compared to intra-vesicular
• Abnormal descent of neck of bladder = negative urethral closure pressure
• Laxity of sub-urethral support from vaginal wall, levator ani, endopelvic fascia
• Stress incontinence –
- When intravesical pressure exceeds the closing pressure on the urethra
- Childbirth is the most common causative factor, leading to denervation of the pelvic floor, usually during delivery. 

- Oestrogen deficiency at the time of menopause leads to weakening of the pelvic support and thinning of the urothelium. 

- Occasionally, weakness of the bladder neck can occur congenitally, or through trauma from radical pelvic surgery or irradiation. 


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4
Q

What is Stress urinary incontinence (SUI)?

A

involuntary leakage of urine on effort or exertion, or on sneezing or coughing. Relaxed pelvic floor. Increased abdominal pressure.

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5
Q

What is Urodynamic Stress Incontinence (USI)?

A

Leakage of urine due to an increase of intra-abdominal pressure in the absence of detrusor activity (50% of female incontinence).
Unlike SUI, USI can only be diagnosed by urodynamic testing

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6
Q

What is urge incontinence?

A
Overactive bladder
 ( – Chronic condition, defined as urgency, with or without urge incontinence, usually with frequency or nocturia. Caused by detrusor over activity, diagnosis made by urodynamic testing. Incidence increases with age. Most common cause of incontinence in older women. Bladder oversensitivity. Neurological disorders
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7
Q

What is Overflow Urinary incontinence?

A

Outflow obstruction or retention
• Acute – overwhelms sphincter
• Chronic - stretches the detrusor and damages it so over time can be incontinent. Causes include neuronal, obstruction or pharmacological
Urethral blockage, bladder unable to empty properly.

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8
Q

What are Congenital causes of Urinary incontinence?

A

bladder exstrophy and ectopic ureter

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9
Q

What do you find when taking the history of Urinary incontinence?

A

• Presenting complaint – onset, duration, SEVERITY on QoL
 Urological Sx – incontinence (inc. volume + frequency), frequency, urgency, nocturia, dysuria, foul smell, poor stream, straining, prolonged/incomplete emptying, dribbling, UTIs, nocturnal enuresis/childhood problems, retention, catheterization/past Rx, faecal incontinence, haematuria
 Colorectal symptoms
 Genitourinary prolapse (lump, dragging, sitting on football)
• Gynae Hx – LMP, menstrual Hx, general, surgery (prolapse/other gynae)
• Obstetric – parity, MOD, birth weights, ages
• Past medical
o Respiratory (cough); Cardiac; GI (constipation); CNS; Diabetes; Psychiatric. Neurology (MS) Anything that increases intra-abdominal pressure. Anaesthetic requirements
• Drug
o Diuretics; Beta-Blockers; Anti-Cholinergics (for urge incontinence)
• Social
• Impact on ADLs, smoking, alcohol, caffeine, carbonated drinks, volume of FLUID INTAKE, prev. ketamine use, heavy lifting at work
• Systemically unwell – UTI?
o Quality of life assessment – Stop them from going to work?
o Can fill in a frequency/ volume chart

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10
Q

What do you find when taking an Examination of Urinary incontinence?

A

• General examination 

o Weight (BMI= incontinence/prolapse. And also surgery less successful)), BP, urinalysis.
o Check for signs of systemic disease. 

o Mobility and mental state. 

o Motivation and manual dexterity. 

o Neurological examination, if there are any symptoms that point to a 
possible neurological cause. 

• Abdominal examination
o Exclude an abdominal or pelvic mass (cysts, retention, fibro uterus and pregnancy-= pressure on bladder)
o Exclude a full bladder (obstruction/retention). 

• Pelvic examination 

o Condition of the vulval skin (any atrophy, erythema, or oedema). 

o Presence and degree of any concurrent uterovaginal prolapse. 

o Assessment of urethral and bladder neck descent on straining. 

o Assessment of pelvic floor muscle strength
o Post menopausal atrophy
o Vaginal discharge
o Ask patient to bear down/cough
• Prolapse – cystocele/urethrocele
• Incontinence
• Speculum and bimanual
• Sims speculum for prolapse
• Rectal examination can evaluate rectal sphincter tone or the presence of fecal impactation

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11
Q

What are the investigations for stress incontinence?

A

• Urinalysis – rule out UTI, DM, bladder malignancy (haematuria); if +ve: MSU MC&S
• Pad test
• Bladder diary
o volume intake and voids – Indicates bladder capacity, frequency and drinking habits. More than 7 voids a day per day = frequency.
• Residual check USS/catheterisation
• MRI
– for prolapses
• Urodynamic testing
• Intra-venous pyelogram – indicates presence of a fistula
• Cystourethroscopy (+ biopsies) – exclude malignancy/stones
o Indications for cystourethrothroscopy –
- Recurrent UTIs, haematuria, bladder pain, suspected urinary tract injury or fistula, exclude bladder tumour or stones, if interstitial cystitis is suspected.

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12
Q

What are the indications for imaging of Urinary incontinence?

A
– USS and MRI
•	Recurrent UTIs
•	Haematuria
•	Urethral diverticula, which need to be differentiated from paravaginal cysts

•	Suspected ureteric injuries
•	Suspected urethral or vesical fistulae

•	Suspected malignancy or renal stones 

*More notes on urodynamics
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13
Q

What is the Management for stress urinary incontinence?

A

Try conservative management first; – 3 month follow-up
• Lifestyle interventions – weight reduction if BMI >30, smoking cessation, treatment of chronic cough and constipation
• Pelvic floor muscle training: 1st line. For at least 3mths should be considered as the first-line treatment:
o physiotherapists usually individualize the programme, but 3 sets of 
8–12 slow maximal contractions sustained for 6–8s each per day is 
a common regimen 

o the exercises need to be continued long term. 

• Biofeedback: refers to the use of a device to convert the effect of pelvic floor contraction into a visual or auditory signal to allow women objective assessment of improvement. 

• Electrical stimulation: can assist in production of muscle contractions in women who are unable to produce muscle contraction. 

• Vaginal cones: have been developed as a way of applying graded resistance against which the pelvic floor muscles contract.
• Pharmacological management of SUI 

o Duloxetine: is the only medical treatment for moderate to severe SUI
 It is an SNRI that enhances urethral striated sphincter activity via a 
centrally mediated pathway
 not recommended for first-line use by NICE = suicidal risk + withdrawal Sx
• Surgery – transvaginal tape: S/E = mesh erosion, infection and dyspareunia

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14
Q

What are the Indications for conservative treatment of stress urinary incontinence?

A
  • Mild or easily manageable symptoms

  • Family incomplete
  • Symptoms manifest during pregnancy
  • Surgery contraindicated by co-existing medical conditions
  • Surgery declined by patient
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15
Q

What are the Investigations for urge incontinence?

A

• Urine culture
o Exclusion of infection is mandatory, as symptoms overlap those of UTI.
• Frequency/volume chart 

o Typical features are i diurnal frequency associated with urgency and episodes of urge incontinence
o Nocturia is a common feature of OAB
• Urodynamics
o Characterized by involuntary detrusor contractions during the filling phase of the micturition cycle, which may be spontaneous or provoked
o Video-urodynamic testing is more appropriate in women with neurological diseases, to exclude vesicoureteric reflux or renal damage secondary to a persistent significant rise in intravesical pressure. 


*Urodynamic assessment is essential for the diagnosis of OAB in women with multiple and complex symptoms. Other factors, such as metabolic abnormalities (diabetes or hypercalcaemia), physical causes (prolapse or faecal impaction), or urinary pathology (UTI or interstitial cystitis), need to be excluded before the diagnosis of OAB is made.

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16
Q

What is the Management for urge incontinence?

A

Conservative management
Behavioural therapy
• Advice to consume 1–1.5L of liquids per day. 

• Avoid caffeine-based drinks (tea, coffee, cola) and alcohol. 

• Various drugs, such as diuretics and antipsychotics, alter bladder function and should be reviewed. 


Bladder retraining/pelvic muscle training
• ability to suppress urinary urge and extend the intervals between voiding. 


Medical management – 3 month follow-up
Anticholinergic (antimuscarinic) drugs
• Block the parasympathetic nerves, thereby relaxing the detrusor muscle. 

o Patients should be advised about the side effects before starting treatment  can’t see, can’t pee, can’t shit, can’t spit
o Contraindications to anticholinergics - • Acute (narrow angle) glaucoma.
• Myasthenia gravis.
• Urinary retention or outflow obstruction. • Severe ulcerative colitis.
• Gastrointestinal obstruction.
Oestrogens

• Treatment with vaginal oestrogen often helps with symptoms of urgency, urge incontinence, frequency, and nocturia. 

Surgery – Reserved as a last resort: cystoscopy and botox; percutaneous sacral nerve stimulation; augmentation cytoplast and urinary diversion

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17
Q

What is Urogenital prolapse?

A

(causes STRESS incontinence)
A prolapse is a protrusion of an organ or structure beyond its normal confines. 50% of parous women have a degree of prolapse – 10-20% seek help.

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18
Q

What is the Classification of Urogenital prolapse?

A
  • Anterior vaginal wall prolapse
  • Urtherocele – urethral decent
  • Cystocele – bladder decent
  • Cystourethrocele – bladder and urethral decent
  • Posterior vaginal wall prolapse
  • Rectocele – rectal decent
  • Enterocele – small bowl decent, pouch of douglas
  • Apical vaginal prolapse (mid compartment)
  • Uterovaginal – uterus out of the vagina – see cervix – dirt
  • Vault – post-hysterectomy inversion of the vaginal apex. No uterus just a rectangular chunk
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19
Q

What is the Grading of Urogenital prolapse?

A

Baden – Walker classification: POPQ
1st degree: the lowest part of prolapse descends halfway down the vaginal axis to the introituse.
2nd degree: the lowest part of the prolapse extends to the level of the introituse and through the introituse on straining
3rd degree: the lowest part of the prolapse extends through the introituse and lies outside the vagina (halfway past intraoitus).

4th degree: max. possible descent = procidentia

Beecham classification 
•	3 degrees of prolapse.
•	1st degree: descent within the vagina
•	2nd degree: descent into the introitus
•	3rd degree: descent outside the introitus (third degree uterine prolapse = procidentia)
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20
Q

What is Anterior Urogenital prolapse?

A

• Anterior vaginal wall prolapse
• Urtherocele – urethral decent
• Cystocele – bladder decent
• Cystourethrocele – bladder and urethral decent
Symptoms: Urinary symptoms (stress IC, urinary frequency)

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21
Q

What is Central Urogenital prolapse?

A

Cervix/uterus

Symptoms: Bleeding/discharge from ulceration associated with procidentia

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22
Q

What is Posterior Urogenital prolapse?

A

• Rectocele – rectal decent
• Enterocele – small bowl decent, pouch of douglas
Symptoms: Bowel symptoms, feeling of incomplete evacuation and something having to press the posterior wall backwards to pass stool

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23
Q

What do you find when taking a History of Urogenital prolapse?

A
  • Dragging sensation – worse at end of day or standing up
  • Non-specific symptoms including local discomfort, lump present, bleeding / infection if ulcerated, dyspareunia
  • Can get specific symptoms depending on where the prolapse is;
  • Rectocele get constipation, incomplete bowl emptying and passive anal incontinence.
  • Cystocele or urethrocele get urinary frequency and urgency, voiding difficulty, UTIs and stress incontinence.
  • Prolapse may require reducing in order to pass urine or stool
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24
Q

What do you find when taking an Examination of Urogenital prolapse?

A
  • Abdominal and bimanual to examine pelvic masses
  • Do a vaginal examination to see extent of prolapse and grade it
  • Assess anterior and posterior vaginal walls and cervical descent with a sims speculum.
  • Ask patient to bear down
  • Can do a combined rectal and vaginal digital examination to aid differentiation between a rectocele and an enterocele – finger will be seen bulging in rectocele
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25
Q

What are the Investigations of Urogenital prolapse?

A
  • If urinary symptoms exclude UTI on dipstick
  • Pelvic USS if pelvic mass suspected
  • ECG, CXR, FBC and U&Es to assess fitness for surgery
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26
Q

What is the Management of Urogenital prolapse?

A

• Prevention – weight loss, avoid heavy lifting, pelvic floor exercises, avoid obstructed labour, adequate suturing of pelvic lacerations, avoid prolonged 2nd stage
• Conservative:
o Ring pessary or shelf pessary - if not sexually active (shelf; if sexually active  ring), not fit for surgery or do not want surgery
• May require topical oestrogens in post-meopausal women to prevent ulceration
• May cause pain, urinary retention, fall out, infection
• Pelvic floor exercises
• Loss weight <30 BMI and stop smoking
• Bladder training – hold on urine for 10 minutes before urinating.
• Fluid and diet management - You may need to cut back on or avoid alcohol, caffeine or acidic foods.
• Surgical – 30% recurrence
• Cystourethrocele: Do an anterior repair (colporrhaphy), or a colposuspension
• Rectocele: Do a posterior repair (colporrhaphy)
• Uterovaginal: Do a sacrohysteropexy (AKA Manchester repair, lift it back up and attach to sacrum), or a hysterectomy in major grades (consider fibroids/ ovarian cancer mass pushing it down or whether bowel is likely to be adhered to uterus)
• Vault prolapse - Sacrospinous fixation/sacrospinous colpopexy (suspend vault to sacrospinous ligament), vaginal mesh
• Vaginal mesh repairs – improves strength and support (increased risk of complications: mesh erosion, infection, dyspareunia – not being used now)
• No surgery with BMI >30

Total vault prolapse condition refers to complete eversion of the vagina following a hysterectomy..

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27
Q

Why should you offer chest XRAYs in Gynaecology Cancers?

A

*Gynae cancers spread to the lung so offer CXR’s
• 10% of female cancers (2nd commonest)
• Cancer - Peak 35-44 and 75-85
• CIN peak – 25-29

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28
Q

What is the Aetiology of cervical cancer?

A
  • HPV 16 and 18, 31, 33
  • 80% of adults who are sexually active have had HPV infection, 70% of infections resolve in one year but some go onto develop CIN
  • Produce proteins E6 and E7 that turn off tumour suppressor genes
  • Risks = unprotected sex and previous STI
  • Smoking – immunosuppressive and a cofactor with HPV for developing cancer
  • Immunosuppression – AIDS etc
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29
Q

What is the Pathophysiology cervical cancer?

A

• Cervix has two epithelia the columnar in the endocervix and the stratified squamous in the vaginal portion. Where they meet is the squamocolumnar junction
As girls go through puberty oestrogen production increases and this junction moves outwards in a process called eversion, the columnar epithelia get exposed to acid of the vagina and undergo physiological metaplastic change into squamous epithelia. So the columnar goes to squamous (this change is part of normal physiology). The area of columnar tissue in the centre of the cervix is known as an ectopy or ectropion.
Transformation zone is where this change happens. If HPV is present this metaplastic change can turn oncogenic as virus DNA is incorporated into transformation zone and cause cervical intraepithelial neoplasia. (CIN occurs at the transformation zone.) This CIN can go on further to progress to cervical carcinoma
• Human papillomavirus
o More than 100 types
o 40 types can infect the genital tract
o All sexually active women are exposed to HPV
o Most HPV infections in young women are temporary and have little long-term significance
o 70% of infections spontaneously resolve in 1 year
o 90% in 2 years

30
Q

What is the Pathology of cervical cancer?

A
  • 90% squamous cell carcinomas

* 10% adenocarcinomas – worse prognosis, not detected by smears

31
Q

What is the Screening of cervical cancer?

A

• Cervical smear + liquid based cytology
o Remove thin layer of cells, examine microscopically for any cells with dyskaryosis
o HPV and chlamydia can be tested for simultaneously

32
Q

What is Dyskaryosis and CIN ?

A

Dyskaryosis – Assessment of dyskaryosis is based on nuclear enlargement, variation in size and shape of the nuclei, hyperchromasia and reduction in the amount of cytoplasm altering nuclear:cytoplasmic ratio.

Dyskaryosis and CIN –
• Dyskaryosis – cytopathological diagnosis
• CIN – histological diagnosis
• Mild dyskaryosis suggests underlying CIN-1
• Moderate dyskaryosis suggests underlying CIN-2
• Severe dyskaryosis suggests underlying CIN-3

Premalignant stage – CIN 1-3 – depends on the level from the basement membrane involved.
If 1/3 of thickness involved – CIN1
If 2/3 of thickness from BM – CIN2
If all of thickness of epithelium effected – CIN3

33
Q

What does this patient have?
27 year old para 2 attends her GP complaining of bleeding after sex (PCB) for 6 months. Menstrual cycle is regular every 28 days and light but she is also complaining of IMB. She smokes 20/ day and is currently taking microgynon for contraception. She has never had a smear test. She has been sexually active for 10 years and has had 4 partners. She has a past history of genital warts.

A

Cervical Cancer PEAK AGES 35-44, 75-85

34
Q

What are the different types of Cervical Cancer?

A

Different types of tumour – SCC (70%) Adenocarcinoma. Adeno squamous (25%) small cell, TCC

35
Q

What are the Risk factors of Cervical Cancer?

A
  1. Persistence of HPV infection (16 and 18) – HPV causes the production of 2 proteins known as E6 and E7 which turn off some tumor suppressor genes
  2. Smoking
  3. Unprotected sexual intercourse
  4. Multiple sexual partners/ partners of promiscuous males
  5. Heterosexual women
  6. Lower social class
  7. Previous STI (HPV)
  8. HIV – immunocompromised
  9. On immunosupressants – transplant recipient
  10. Slight – COCP
  11. Non-attendance at cervical screening programme
36
Q

What are the clinical features of Cervical Cancer?

A

History:
• Post-coital bleeding, inter-menstrual bleeding and postmenopausal bleeding
• Persistent, offensive, blood-stained discharge
• Pain in late disease (Pain- loin (obstructed ureter), buttock and back- metastatic)
• Swollen leg- thrombosis in the pelvis
• Renal failure
Examination:
• Speculum examination
• Bimanual examination
• PR

37
Q

What are the investigations for Cervical Cancer?

A

• Colposcopy
o Examination of cervix with bright light and magnification to identify any abnormal area.
o The who transformation zone should be identified.
• Cervical biopsy
• FBC, U&Es, LFTs
• MRI pelvis – assess tumour volume, size, local invasion and pelvic node spread.
• CT abdomen and chest (or CXR) – for distant spread
• Liquid based cytology
o Remove thin layer of cells, examined microscopically for any cells with dyskaryotic features.
o HPV and chlamydia can be tested for simultaneously

38
Q

What is the Spread of Cervical Cancer?

A
  • Direct or local – vagina, bladder, parametrium, bowel
  • Lymphatic – parametrial nodes, internal, external and common illiac nodes, obturator nodes, pre-sacral and para-aortic nodes
  • Bloodborne – lungs and liver
39
Q

What is the Staging of Cervical Cancer?

A

FIGO staging 2010
• Stage 1 : Carcinoma confined to the cervix
• Stage 2 : Carcinoma spread outside of the cervix and into the upper 2/3’rds of the vagina and the parametrium (separates cervix and bladder)
• Stage 3: Involves the lower 1/3rd of the vagina or the pelvic side wall. Can have ureteric obstruction at this point and hydronephrosis from it.
• Stage 4: Involvement of bladder or rectum or distant metastasis

40
Q

What is the treatment for Cervical Cancer?

A
  1. CIN2/3 = LLETZ (large loop excision of transformation zone/loop diathermy)
    • Complication: pre-term labour
    . Want children + stage 1 + Occult carcinoma – very early.
    • Cone biopsy and laparoscopic pelvic node dissection.
    • Pre-term labour and post-op haemorrhage are complications
  2. Want children + stage 1 + not occult (clinical carcinoma)
    • Trachelectomy (fertility sparing) and pelvic node dissection
     Remove 80% of the cervix and the nodes and place stitch to support cervix (cervical cerclage) – women still can have children but high miscariage rates
    • Only possible if lymph nodes are negative
    • Stage 1b or 2a
    • Hyseterctomy/radical hysterectomy (Werthiems) - including upper 1/3 of vagina and pelvic node dissection. Possible if lymph nodes are negative. Ovaries remain if young
    • Complications include bladder dysfunction and sexual dysfunction.
    • Straight to chemo-radiotherapy if older patients – may have similar survival
  • Stage 2b or worse or positive lymph nodes
  • Radiotherapy and chemotherapy for palliation – platinum agents
  • also do radiotherapy in postmenopausal women with early disease due to the increase likelihood of bladder dysfunction. Initial inflammatory effects of the radiation cause bowl and bladder urgency and then can become fibrosed so permanent dysfunction
  • Follow up 6 weeks post treatment, every 3-4 months for 1-2 years, every 6 moths for a total of 5 years
  • Death commonly due to uraemia from ureteric obstruction
41
Q

What is the Prevention of Cervical Cancer?

A
  • Vaccination
  • Gardasil (Merck) – HPV 16, 18 + 6, 11 (90% genital warts)
  • Cervarix (GlaxoSmithKline) – HPV 16, 18
  • All girls aged 12 to 13 - aim to vaccinate prior to sexual contact
  • Part of the NHS childhood vaccination programme
  • Estimated 400 lives could be saved every year in the UK as a result of vaccinating girls before they are infected with HPV
  • Provides effective protection for at least 8 years after completion of the three-dose course
  • Delivered largely through secondary schools
  • Consists of three injections over a period of 12 months
  • Should prevent 90% of warts and 60-70% of CIN.
  • Screening
  • 3-yearly from 25-50 years (from 20 prior to 2003)
  • 5-yearly from 50-64 years
  • Detects squamous cells carcinomas better than adenocarcinomas
  • Only 25+ as complication from LLETZ – preterm labour and the lesions can regress with out any treatment so danger of over treating. Low chance of cancer under 25
42
Q

What are the Differential Diagnoses of Cervical Cancer?

A

• STI – Chlamydia/ gonorrhoea, hormonal – needs stronger pill dose, cervical polyp, endometrial pathology (rare)

43
Q

What is this?
Case – 75 year old nulliparous woman presents with 3 month history of bleeding on wiping. She has a BMI of 45 is diabetic and hypertensive. Her last smear was normal at 65. She had a background history of PCOS and failed fertility treatment. She has a precious history of breast cancer. Currently medications are verapamil, tamoxifen, metformin.

A

Uterine/endometrial Cancer

  • Most common genital tract cancer
  • 5 year survival
44
Q

What is the Pathophysiology of Uterine/endometrial Cancer?

A
  • OESTROGEN:PROGESTERONE RATIO
  • Unopposed oestrogen leads to endometrial hyperplasia – proliferation/thickening which gives a greater chance of cancer developing. Causes atypical hyperplasia which is pre-cancerous
  • Atypical hyperplasia is precancerous and develops into invasive cancer 10-50% over 20 years
  • Simple, complex or atypical
  • Unexposed oestrogen can occur from a variety of sources but after menopause don’t get progesterone or oestrogen, but postmenopausal, oestrogen can arise from break down of fats etc, therefore having an oestrogenic effect on the endometrium and wont have progesterone to protect the lining
  • Most of the uterine cancers arise from the endometrium,
  • 90% are adenocarcinoma of columnar endometrial gland which are classed as type 1
  • Can be serous papillary carcinomas, which are type 2.
  • Adenocarcinomas are oestrogen dependent, occur in younger women and have a better prognosis
  • Serous papillary carcinomas occur in elderly women, non-oestrogen dependent and they have a poor prognosis.
  • Clear cell carcinomas also arise from the endometrium but are rare
  • Can get malignancy from the stroma or myometrium which are sarcomas
45
Q

What are the Risk factors of Uterine/endometrial Cancer?

A
  • Obesity (~1/3 of all cases)
  • Diabetes
  • Sedentary life-style (23% reduction in risk in active women)
  • Menstrual factors: early menarche, late menopause, low parity
  • Anovulatory amenorrhoea, e.g. PCOS
  • Unopposed oestrogen HRT
  • Oestrogen-secreting ovarian tumours
  • Tamoxifen
  • FH of colorectal, endometrial or breast cancer
  • Smoking slightly reduces the risk
46
Q

What are the Protective factors of Uterine/endometrial Cancer?

A
  • COCP, IUS and progesterone only pill decreases incidence by 50%.
  • Smoking
  • Pregnancy
  • Diet and exercise
  • Reduced menstrual history
47
Q

What are the clinical features of Uterine/endometrial Cancer?

A

History
• PMB – 10% of women with PMB have endometrial cancer
• Pre menopausal - Irregular, heavy or intermenstrual vaginal bleeding, especially if <40 years old
• Blood stained discharge
• Lower abdominal pain
• Dyspareunia
• Symptoms from mets – altered liver function, respiratory symptoms
Examination
• Speculum to exclude other causes such as cervical or vaginal lesions.
• On bimanual can feel a fixed bulky uterus if disease is advanced.
• Smear may show CGIN

48
Q

What are the Investigations of Uterine/endometrial Cancer?

A
  • Transvaginal ultrasound to look for endometrial thickness. If >4mm need to do a hysteroscopy and biopsy, if less than 4mm its unlikely to be cancer
  • Do a biopsy of it via a hysteroscopy and can grade it
  • Pipelle is less invasive – appropriate in lower risk patients
  • If cancer is confirmed do a MRI to show depth of invasion, cervical involvement, lymphadenopathy, metastasis
  • CT abdomen and chest if high-risk cancer, e.g. sarcoma
49
Q

What is the Staging of Uterine/endometrial Cancer?

A

FIGO staging only possible after hysterectomy – surgical, histological and involves LN
• Stage 1 – Confined to uterine body – 75% of patients
• Stage 2 - Tumour invading cervical stroma (remember cervix part of uterus)
• Stage 3 – Spread outside of the uterus
• Stage 4 – Tumour invaded bladder or bowl or distant mets

50
Q

What are the Different types of Uterine/endometrial Cancer?

A
  • Adenocarcinoma is commonest (90%) – endometrioid type
  • Serous papillary carcinoma (5%)
  • Clear cell carcinoma(4%)
  • Sarcomas
51
Q

What is the Spread of Uterine/endometrial Cancer?

A
  • Myometrium acts as a barrier for spread. So there is early presentation and less likely to have spread on presentation.
  • Direct – cervical stroma, vagina, fallopian tubes and ovaries
  • Across peritoneal cavity to omentum, surface of other organs – liver, bowel
  • Lymphatic – pelvic, para-aortic and rarely inguinal lymph nodes
  • Blood-borne – liver, lungs – late
52
Q

What is the Management of Uterine/endometrial Cancer?

A
  • Total hysterectomy, bilateral salpingo-oophorectomy, peritoneal washings in stage 1
  • Give post-operative radiotherapy if lymph node involvement/later stage
  • High dose progestogens – useful in palliation, recurrences, may reverse pre-malignant phase
53
Q

What are the Differential Diagnoses of Uterine/endometrial Cancer?

A

endometrial polyps, cervical pathology, urogenital pathology – stones, bladder tumour, STI, Vaginal infection, BV etc

54
Q

What is this ?
Case – 55 year old para 2 presents with weight loss, anorexia, mild abdominal pains and abdominal distension over the last 4 months. She underwent IVF with twins at the age of 50 after 25 years of failed IVF attempts. Her mum and maternal aunty were diagnosed in their 40’s with breast cancer.

A

Ovarian Cancer

55
Q

What is the Epidemiology of Ovarian Cancer?

A
  • Most common cause of gynae cancer death as it presents late and non specific symptoms
  • Seen in higher socioeconomic groups as having babies is protective.
  • 85% in women over 50yrs
56
Q

What is the Pathophysiology of Ovarian Cancer?

A
  • Oestrogen and gonadotrophin secretion will cause epithelial proliferation (during ovulation/menstruation)
  • Epithelial ovarian cancers = 80%, as it’s a reproductive organ there can be sex cord stromal tumours and germ cell tumours.
  • Epithelial – derived from Mullerian epithelium. Serous adenocarcinomas
  • Sex cord or stromal – derived from ovarian stroma, sex cord derivatives or both
  • Germ cell – most common in women <30yrs - derived from ovarian germ cells (including teratomas)
57
Q

What are the Risk factors of Ovarian Cancer?

A
  • Nulliparity
  • HRT
  • Endometriosis
  • Difficulties conceiving
  • 5-10% of patients with epithelial ovarian cancer have a genetic predisposition: BRCA1 and BRCA2 gene mutations
58
Q

What are the clinical features of Ovarian Cancer?

A

History (up to 15% of patients will remain asymptomatic at diagnosis)
• Weight loss, anorexia
• Non specific and vague symptoms including, ABDOMINAL DISTENTION AND BLOATING. Persistent pelvic and abdominal pain and loss of appetite and feeling full quickly.
• Also get pressure effects on the bladder and rectum causing urinary problems and bowl problems,
• Dyspnoea - from pleural effusions
• Abnormal vaginal bleeding and back ache
• Differential diagnosis is IBS so suspect this in IBS women.
o Other DDx - Primary peritoneal carcinoma/ ascites – liver alcohol, IBS,IBD, benign ovarian cyst – dermoid, endometroima
• Spreads to the peritoneum so can present with ascites

Examination
• Adnexal or pelvic mass, shifting dullness, irregular abdominal mass = omental cake, enlarged nodes, cachexia
• Breast/GI mets?
• 75% of cases of ovarian cancer present as Stage III or IV disease
*Typically presents late – 75% of cases present as stage III or IV

59
Q

What is the Staging of Ovarian Cancer?

A
  • Stage I – limited to one or both ovaries
  • Stage II – pelvic extension or implants but still within pelvis
  • Stage III – microscopic peritoneal implants outside of the pelvis; or limited to the pelvis with extension to the small bowel or omentum
  • Stage IV – distant metastases
  • Spreads via transcoelomic spread – within pelvis and abdomen
60
Q

What are the investigations of Ovarian Cancer?

A
  • Pelvic ultrasound – look for mass and ascites,
  • Solid, spectate mass indicates malignancy
  • CA125 – Serous, endometrioid cancers – not specific
  • Expressed in 80% of ovarian Ca
  • Expressed in 50% at early stage
  • Also elevated in endometriosis and ascites
  • CA19.9 – Mucinous – epithelial stromal tumours
  • Testing for pancreatic mets
  • Carcinoembryonic antigen – CEA AFP, HCG, LDH – tumour markers
  • Testing for bowel mets
  • Chest X-ray
  • FBC, U&Es, LFTs
  • CT abdomen and pelvis
  • Paracentesis of ascites – if malignant cells found disease is at least stage 1c and patient will require chemo
  • Laparoscopy
61
Q

What is the Treatment of Ovarian Cancer?

A
  • TAH, BSO, omentectomy, lymph node sampling and peritoneal biopsies with peritoneal washings or ascitic fluid obtained for cytology
  • Adjuvant chemotherapy with platinum (carboplatin) based compounds has been shown to benefit women with no residual disease following surgery
  • If spread can do debulking, resection of bowl, peritoneal stripping or splenectomy. Need to do lymph node resections as well.
  • Cant screen for it and no premalignant condition
  • May monitor CA-125 for recurrence
62
Q

What is this?
Case – 70 year old smoker who presents with a sore, itchy vulva with a mass on her left labia majora. She has a background history of lichen sclerosis (chronic vulval skin condition) and SLE (stable). She has previously had CIN 2 on a smear test, which was treated with LLETZ.

A

Vulval Cancer
• Vulva includes labia clitoris and perianal and mons pubis.
• 95% Squamous cell carcinomas. Spreads to the inguinal and femoral nodes and then up the lymphatic chain and into liver and lungs
• Disease of post menopausal women

63
Q

What is the Aetiology of Vulval Cancer?

A
  • Bit like cervical cancer as you get VIN, it also occurs de novo though
  • In young women get it from HPV 16 and 18,
  • In older women get it form dermatological causes so from lichen sclerosis which progresses from dermatitis and lichen planus. Known as vulvodermatosis
64
Q

What are the clinical features of Vulval Cancer?

A

History
• Vulval symptoms –
o lump, pain, bleeding, cauliflower growths, ulcerate, pruritis, discharge
o Can be asymptomatic
• Often late presentation as not seen/embarrassed
Examination
• Mass/ulcer most commonly on labia majora or clitoris. Hard inguinal lymph nodes. Skin thicker and lighter/darker = VIN
• DDX
o bartholins cyst, lichen scherosis lesion

65
Q

What are the Risk Factors of Vulval Cancer?

A
  • Age – 50% over the age of 70.
  • HPV – 16,18,31,33
  • Smoking
  • Immunodeficiency – HIV, immunosuppressants
  • Lichen schlerosis – 4% risk of vulvar cancer
  • Melanoma – personal or family history
  • Paget’s disease of the vulva
66
Q

What are the Investigations of Vulval Cancer?

A
•	Biopsy – diagnosis is made by biopsy 
o	Histology – 
	Squamous Cell Carcinoma - 90%
	Adenocarcinoma
	Melanoma
	BCC
	Verrucous carcinoma and sarcoma
•	Examination to asses direct spread – PR, PV, Inguinal lymphadenopathy
•	CXR/MRI – mets
•	CT scan pelvis and abdomen 
•	Colposcopy +/- smear
67
Q

What is the Staging of Vulval Cancer?

A
  • Stage 1 – confined to vulva or perineum <2cm
  • Stage 2 – confined to vulva or perineum >2cm
  • Stage 3 – extends beyond the vulva and perineum to urethra, vagina or anus OR unilateral regional lymph node
  • Stage 4 – distant mets OR bilateral pelvic nodes OR involves mucosa of rectum, bladder, upper urethra or pelvic bone
68
Q

What is the Prognosis of Vulval Cancer?

A
  • 5yr survival
  • Stage 1 – 90%
  • Other stages – 40%
  • Distant Mets – 16%
69
Q

What are the Premalignant conditions of Vulval Cancer?

A

Squamous cell carcinoma forms over many years. Premalignant phase is VIN - vulvar intraepithelial neoplasia. “Intraepithelial” means that the abnormal cells are only found in the surface layer of the vulvar skin (epithelium).
Treatment = local excision, laser therapy, topical immunomodulators

70
Q

What is the Treatment of Vulval Cancer?

A
  • Surgery:
  • Stage 1a – wide local excision
  • Other stages – triple incision vulvectomy / sentinel groin lymph node dissection
  • Intimate and destabilizing sensitive surgery like genital mutilation.
  • Chemoradiotherapy may be used prior to surgery, post-op for lymph nodes or for palliation