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Gynaecology Pt. 3 Flashcards

1
Q

What is endometrial cancer?

A
  • MOST COMMON type of uterine cancer
  • MOST COMMON gynaecological malignancy
  • Age-related incidence = 95/100,000
  • Mean age of diagnosis = 62 years
  • Arises from glandular component of endometrium
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2
Q

How are endometrial cancers classified?

A
  • Type 1: endometrioid adenocarcinomas
    • Oestrogen-driven
    • Arise from a background of endometrial hyperplasia
  • Type 2: high-grade serous and clear cell carcinomas
    • Arise from an atrophic endometrium

Range from Grades 1-3 (3 = high grade)

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3
Q

What is the aetiology of endometrial cancer?

A
  • Oestrogen causes proliferation of endometrial cells
  • Progesterone can inhibit this effect
  • Obesity is a major risk factor because women who are obese are more likely to have anovulatory menstrual cycles and less likely to get pregnant
    • In addition, aromatisation of androgens to oestrogen in adipose tissue provides a continuous postmenopausal supply of oestrogen
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4
Q

What are risk factors for endometrial cancer?

A
  • Obesity
  • Diabetes
  • Nulliparity
  • Late menopause > 52 years
  • Unopposed oestrogen therapy
  • Tamoxifen therapy (anti-oestrogenic in the breast but stimulatory in the endometrium)
  • Family history of colorectal and endometrial cancer
    • Lynch syndrome (caused by mutations in mismatch repair genes)
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5
Q

What are protective factors against endometrial cancer?

A
  • Hysterectomy
  • COCP
  • Progestin-based contraceptives, including injectables
  • IUS (Cu-IUD, LNG-IUD)
  • Pregnancy
  • Smoking
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6
Q

Describe prevention for endometrial cancer

A
  • Hormonal contraceptives and IUDs reduce the risk of ovarian cancer
  • Women with Lynch syndrome will be offered prophylactic hysterectomy following completion of family
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7
Q

What are clinical features for endometrial cancer?

A
  • Postmenopausal bleeding
    • This is a RED FLAG that should be taken seriously
    • Inspect the external genitalia and perform a speculum examination to rule out vulval, vaginal and cervical cancer
    • Physical examination may be NORMAL
    • Diagnosis can only be excluded with TVUSS, hysteroscopy and endometrial biopsy
    • Benign causes of PMB:
      • Unscheduled bleeding on HRT
      • Atrophic vaginitis
  • Abdominal pain
  • Urinary dysfunction
  • Bowel disturbance
  • Respiratory symptoms
  • May be detected incidentally on cervical smear (abnormal glandular cytology)
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8
Q

How is endometrial cancer investigated and diagnosed?

A
  • TVUSS
    • Allows assessment of endometrial thickness
    • If < 4 mm = endometrial cancer is very unlikely
    • If > 4 mm = requires further evaluation by hysteroscopy and/or biopsy
  • Hysteroscopy
    • Performed under local anaesthetic in the outpatient setting where possible
    • General anaesthetics may be used if cervical stenosis or if hysteroscopy is poorly tolerated
    • A biopsy can be taken for histological analysis
    • Complex hyperplasia with atypia is a premalignant condition that often co-exists with low-grade endometrioid tumours of the endometrium
      • 25-50% risk of progression to endometrial cancer
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9
Q

How is endometrial cancer staged?

A
  • Determined by MRI
  • FIGO staging
  • Patients with high-grade tumours will under CT-TAP to exclude distant metastases
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10
Q

What can the management of endometrial cancer be split into?

A
  • Surgery
  • Adjuvant Treatment
  • Hormone Treatment
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11
Q

What is the surgical management of endometrial cancer?

A
  • Mainstay of treatment for endometrial cancer
  • Extent depends on grade, stage and co-morbidities
  • Standard surgery: total hysterectomy with bilateral salpingo-oophorectomy
  • This can be abdominal or laparoscopic
  • If the MRI is suggestive of cervical involvement, a modified radical hysterectomy is performed
  • If high-grade or type 2 histology, pelvic and para-aortic node dissection may be performed in some centres
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12
Q

What is adjuvant treatment of endometrial cancer?

A
  • Postoperative radiotherapy reduces local recurrent rate but does NOT improve survival
  • Local radiotherapy or brachytherapy are options
  • Chemotherapy is used for advances or metastatic disease (little evidence to support its use)
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13
Q

What is the hormone treatment of endometrial cancer?

A
  • High-dose oral or intrauterine progestins
  • Useful for women with complex atypical hyperplasia and low-grade stage 1A endometrial tumours
  • Relapse rates are high
  • May be suitable for women who are not fit for surgery or want to avoid surgery for fertility reasons
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14
Q

How does endometrial cancer affect fertility?

A
  • Primary infertility due to PCOS is a risk factor for pre-menopausal endometrial cancer
  • Alternatives to hysterectomy for pre-menopausal women are only possible for pre-cancer or early-stage low-grade endometrial cancers
  • Hormone therapy (oral progestogens or LNG-IUS) is associated with moderate response and high relapse rates
  • Women faces with losing their fertility should be referred to a specialist to discuss ovarian conservation and/or stimulation for egg retrieval and surrogacy
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15
Q

What is the prognosis of endometrial cancer?

A
  • 5-year survival = 80%
  • Dependent on type, stage and grade
  • Bad prognostic features:
    • Age
    • Grade 3 tumours
    • Type 2 histology
    • Deep myometrial invasion
    • Lymphovascular space invasion
    • Nodal involvement
    • Distal metastases
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16
Q

What are sarcomas of the uterus?

A
  • 5% of uterine cancers
  • Pure Sarcomas
    • Endometrial stromal sarcomas
    • Leiomyosarcoma
      • From the myometrium
      • Rarely associated with malignant transformation of benign fibroids
      • Present with rapidly growing pelvic mass and pain
    • Surgery is the mainstay of treatment
  • Mixed Epithelial Sarcomas (Carcinosarcomas)
    • Contain both carcinomatous and sarcomatous elements
    • Most present after menopause
    • Post-menopausal bleeding
    • Treated by surgery followed by post-operative radiotherapy
  • Heterologous Sarcomas
    • Consists of sarcomatous tissue not usually found in the uterus (e.g. striated muscle, bone and cartilage)
    • Most common is rhabdomyosarcoma
    • May present in children
    • High recurrent rates with distant metastases
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17
Q

What is the aetiology of cervical cancer?

A
  • Low risk HPV = 6 + 13
  • High risk HPV = 16 + 18
  • 80% of adults show serological evidence of previous HPV infection
  • Infection is usually transient with no clinical consequences
  • A minority will develop a persistent genital infection that predisposes them to premalignant and malignant change
  • Smoking increases the risk of persistent HPV infection
  • HIV and immunosuppressed patients are at particular risk of developing cervical cancer
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18
Q

What is the pathophysiology of cervical cancer?

A
  • The tubular cervix consists of stromal tissue covered by:
    • Squamous epithelium - in the vagina (ectocervix)
    • Columnar epithelium - in the cervical canal (endocervix)
  • Endocervix has deep folds (crypts) that are lined by columnar epithelium
  • The meeting of the two types of epithelium is the squamocolumnar junction (SCJ)
  • The position of the SCJ varies throughout life
    • In CHILDREN it lies in the external cervical os
    • At PUBERTY it extends outwards onto the ectocervix
    • In ADULT LIFE it returns to the external cervical os through the process of metaplasia
  • The transformation zone (TZ) is the area between the original SCJ and the current SCJ where the epithelium changes from columnar to squamous over time
    • This is the site where malignancy and pre-malignancy develop
  • Persistent HPV infection triggers oncogenic processes in the TZ
  • Integration of HPV DNA into the basal epithelial cells leads to immortalisation and rapid cellular turnover
  • Disordered immaturity within the epithelium is called cervical intraepithelial neoplasia (CIN)
    • Immature cells are:
      • Hyperchromatic
      • Large nuclei
      • Minimal cytoplasm
      • Abnormal mitotic figures
    • Classified as CIN1, CIN2 or CIN3
      • CIN2 and 3 are considered ‘high grade’
  • Natural History of CIN
    • Can regress or progress
    • Low-grade disease is more likely to spontaneously regress
    • High-grade disease requires treatment (20% risk of progression to cancer)
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19
Q

How is cervical cancer investigated and diagnosed?

A
  • Cervical cytology
  • HPV Testing in Cervical screening
  • National Cervical Screening Programme
  • Colposcopy
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20
Q

What is cervical cytology?

A
  • Liquid-based cytology (LBC) is a technique by which a small brush is used to sample cells from the TZ and the brush head is placed in a fixative
  • The cellular aspect from this sample is viewed under the microscope
  • Abnormal cervical cytology shows squamous cells at different stages of maturity (dyskaryosis)
  • Cervical cytology can be classified as:
    • Normal
    • Low grade - minor cytological abnormalities showing mild dyskaryosis and or borderline change
    • High grade - moderate and severe dyskaryosis
  • NOTE: there is some correlation between cytology grade and CIN grade but this is NOT totally reliable
  • Cervical cytology allows triaging of patients to the colposcopy clinic for further assessment
  • 95% of women will have normal cervical cytology
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21
Q

What is the role of HPV testing in cervical screening?

A
  • High-risk HPV screening improves sensitivity of cervical screening
  • It has a high negative predictive value - i.e. if a woman tests negative for high-risk HPV, they have a very low risk of developing cervical cancer
  • Women with minor cytological abnormalities undergo reflex testing with high-risk HPV
    • Negative - return to routine recall
    • Positive - refer to colposcopy
  • UK is moving towards primary HPV screening - this means testing all cervical cytology specimens for HPV first, then carrying out reflex cytological assessment on any positive samples
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22
Q

What is the National Cervical Screening Programme?

A
  • Started in 1988
  • Age range:
    • 25-64 years = every 3-5 years
  • Coordinated by the National Health Service Cervical Screening Programme (NHSCSP)
23
Q

What is a colposcopy?

A
  • DEFINITION: examination of the magnified cervix using a light source
  • The woman is placed in the semi-lithotomy position
  • A speculum is placed in the vagina and the cervix is examined with a light source
  • Application of acetic acid and iodine solutions highlight abnormal areas of the cervix
    • Acetic acid - areas of increased cell turnover (including CIN) appear white
    • Iodine - areas of CIN lack intracytoplasmic glycogen and, hence, fail to stain brown with iodine
  • CIN can also be classified as low or high-grade based on colposcopy
    • Low-grade - subsequent colposcopy and cytology in 6 months
    • High-grade - treated in clinic on the same visit (‘see and treat’)
    • Biopsies may be taken if unsure
24
Q

What is the management of premalignant disease of the cervix?

A
  • Aim to effectively eradicate CIN (ensuring that post-treatment cytology is negative)
  • High-grade CIN requires treatment with excision or ablation
  • Low-grade CIN regresses spontaneously in up to 60% of cases
    • Requires close follow-up with colposcopy and cytology 6 months after initial diagnosis
  • Loop diathermy (large loop excision of transformation zone (LLETZ)) is the favoured method
    • CIN can develop within the crypts of the epithelium and therefore excisional techniques need to be at least 7 mm deep
    • This only take 15 mins under local anaesthetic
    • 95% of patients will have negative cytology at 6 months
    • Risks
      • Large excision or repeat excisions are associated with an increased risk of midtrimester miscarriage and preterm delivery
  • Other options
    • Cold coagulation
      • Effective but does not provide a specimen
    • Cone biopsy
      • Cuts away part of the cervix but requires general anaesthetic
      • Associated with cervical stenosis and incompetence
      • Superseded by loop diathermy
  • Patients who undergo treatment for CIN will receive a test of cure 6 months later
  • HPV vaccination
    • National vaccination programme for school girls aged 12-13 years
    • Quadrivalent vaccine = 6, 13, 16 and 18
25
Q

What is the presentation of cervical cancer?

A
  • Small volume microscopic disease may be ASYMPTOMATIC
  • Many are picked up incidentally
  • Abnormal bleeding
    • Post-coital bleeding
    • Intermenstrual bleeding
    • Postmenopausal bleeding
  • A pelvic examination should be performed in any patient with these symptoms including visualisation of the cervix
    • May see a cervical mass that bleeds on contact
    • In advanced disease, there may be hardness or fixity of tissues
    • A biopsy should be taken in the outpatient setting
    • NOTE: endophytic tumours are less clinically revealing than exophytic
  • Symptoms of advanced disease
    • Pain
    • Incontinence (vesicovaginal fistulae)
    • Anaemia
    • Renal failure (ureteric blockage)
26
Q

What is the pathophysiology of malignant cervical cancer?

A
  • 70% of cervical cancers are squamous cell carcinomas
  • Adenocarcinomas make up the remainder
  • Adenocarcinomas are less likely to be picked up on screening
  • The precursor to adenocarcinoma, cervical glandular intraepithelial neoplasia (CGIN), can also be detected at colposcopy
    • NOTE: lesions within the endocervical canal may be difficult to visualise
  • CIN and CGIN can co-exist
  • The tumour can grow through the cervix into the parametria, bladder, vagina and rectum
  • Sites of metastasis
    • Pelvic (iliac and obturator) lymph nodes
    • Para-aortic nodes
    • Liver
    • Lungs
27
Q

How is cervical cancer staged?

A
  • FIGO staging
  • Biopsy - confirm malignancy and assess tumour type
  • MRI of abdomen and pelvic allows assessment of spread
  • CXR - check for lung metastases
  • Rectovaginal examination under anaesthetic may be necessary to assess tumour size, fixity and vaginal involvement
  • Cystoscopy may be used to check for bladder involvement
  • Small mobile tumours favour SURGERY
  • Large fixed tumours favour the use of radiotherapy
  • NOTE: staging is largely based on clinical findings rather than surgery and pathology
28
Q

What is the management of malignant cervical cancer divided into?

A
  • Preclinical lesions: Stage 1A
  • Clinically Invasive Cervical Carcinoma: Stages 1B - 4
  • Surgery
  • Radiotherapy
  • Chemotherapy
  • Depends on stage, requirement for future fertility and patient factors
29
Q

What is the management of preclinical lesions (Stage 1A)?

A
  • Microscopic tumours usually picked up as incidental findings
  • Small lesions should be removed with a clear margin and co-existing CIN should also be completely excised
  • For these lesions, local excision with good clear margins is all that is required
30
Q

What is the management of Clinically Invasive Cervical Carcinoma (Stage 1B - 4)

A
  • Tumours are larger so fertility-preserving treatment is more difficult
  • If small volume disease confined to the cervix
    • Radical hysterectomy and bilateral pelvic node dissection (Wertheim’s hysterectomy)
    • If fertility-sparing is required: radical trachelectomy (removal of cervix and upper vagina) and pelvic node dissection
  • NOTE: in Stage 1B disease, pelvic radiotherapy is as effective as surgery
  • If the tumour is beyond the cervix (stage 2-4), radiotherapy is the mainstay of treatment
31
Q

What is the surgical management of malignant cancer?

A
  • Standard operation for stage 1B tumours is radical hysterectomy with pelvic lymph node dissection
  • NOTE: pelvic lymph nodes include obturator, internal and external iliac nodes
  • Ovaries in pre-menopausal women can be spared
  • High cure rate
  • Risks
    • Bladder dysfunction (atony)
      • Common in the immediate post-operative period and may require intermittent self-catheterisation
    • Sexual dysfunction (due to vaginal shortening)
    • Lymphoedema (due to pelvic lymph node removal)
      • Can be managed with leg elevation, good skin care and massage
32
Q

How does radiotherapy manage malignant cancer?

A
  • TWO ways of delivering radiotherapy:
    • External beam radiotherapy
      • Usually given over 4 weeks
      • Each delivery of radiotherapy usually lasts about 10 mins
    • Internal radiotherapy (brachytherapy)
      • Rods of radioactive selenium is inserted, under anaesthetic, into the affected area
      • The effects extend up to 5 mm away from the rod
  • Risks
    • Lethargy
    • Bowel and bladder urgency
    • Skin erythema (external beam radiotherapy)
    • Long-term:
      • Fibrosis
      • Vaginal stenosis
      • Cystitis-like symptoms
      • Malabsorption and mucous diarrhoea
      • Radiotherapy-induced menopause
33
Q

How does chemotherapy manage malignant cancer?

A
  • Usually cisplatin

- Ideally given in conjunction with radiotherapy (improves cure rates)

34
Q

What is the epidemiology and aetiology of malignant disease of the vulva?

A
  • UNCOMMON
  • Mainly affects older women
  • 90% are squamous cell carcinomas
  • Remainder are malignant melanoma, basal cell carcinoma and adenocarcinoma of the Bartholin’s gland
  • TWO types of squamous cell carcinomas of the vulva:
    • High-risk HPV associated
      • Arise on a background of high-grade vulval intraepithelial neoplasia (VIN3)
      • Usually young women
    • Non-HPV associated
      • Usually older women
      • Associated with lichen sclerosus
35
Q

What is the clinical presentation of malignant disease of the vulva?

A
  • Lump or ulcer associated with bleeding or discharge
  • May be painless or painful
  • Examination
    • Well-demarcated raised or ulcerated lesion that is hard and craggy and bleeds on touch
    • Often associated pre-malignant change
      • Younger women - VIN
      • Older women - lichen sclerosus
  • Vulval cancers spread locally and metastasise via the inguinofemoral lymph nodes before the pelvic nodes
36
Q

How is malignant disease of the vulva investigated?

A
  • Specialist gynaecological oncology MDT
  • Biopsy to confirm the diagnosis
  • Examination under anaesthetic may be required to assess suitability to resection
  • CT scan may be required for large tumours with obvious groin node disease and potential distant metastases
  • FIGO staging
37
Q

How is malignant disease of the vulva managed?

A
  • Vulval excision
    • Radical surgical excision aiming for a clear margin of 10 mm is the mainstay
    • If the tumour is close to the urethra or anus it can be more difficult to operate
    • Large lesions may be shrunk with neoadjuvant radiotherapy often with chemotherapy
  • Sentinel Lymph Node Biopsy
    • Untreated groin node biopsies will be fatal
    • Affected nodes cannot be reliably identified with radiology
    • Current approach: full inguinofemoral lymphadenectomy (for all tumours with depth of invasion > 1 mm)
    • NOTE: groin lymphadenectomy is a very morbid procedure with complications including wound healing problems, infection, VTE and chronic lymphoedema
    • Groin nodes are involved in 15% of women with vulval cancer
    • Full groin lymphadenectomy may be avoided by doing a sentinel lymph node biopsy (first node that the area drains to)
    • A dye and radioactive nucleotide can be injected into the vulval tumour to identify the sentinel node
    • If the sentinel node is positive for disease, then full groin lymphadenectomy is indicated
  • Radiotherapy
    • Adjuvant radiotherapy is indicated if the excision margins are close or in the presence of two or more groin node metastases
    • Radical radiotherapy may be used instead of surgery if the patient is unfit for surgery
38
Q

Describe a hysterectomy

A
  • When the uterus is enlarged by fibroids or significant adhesions are expected or it is planned to remove the ovaries, hysterectomy is usually performed abdominally
  • There are THREE pedicles that need to be removed in hysterectomy:
    • Infundibulopelvic ligament (containing ovarian vessels)
    • Uterine artery
    • Angles of the vault of the vagina (containing vessels ascending from the vagina and the ligaments to support the uterus can be taken out with this)
  • If the uterus is a normal size it can be taken out vaginally
  • In prolapse surgery, the uterus is often taken out vaginally
  • Vaginal surgery requires a shorter stay in hospital and less recovery time before full mobility and activity
  • Increasingly, vaginal surgery is being done laparoscopicaly (laparoscopic-aided vaginal hysterectomy)
39
Q

What are the complications of a hysterectomy?

A
  • Haemorrhage
  • DVT
  • New bladder symptoms (overactive bladder and stress incontinence)
  • Early onset of menopausal symptoms
  • Immediate onset of menopausal symptoms
  • Bladder injury
  • Ureteric injury
  • Rectal injury
  • Fistulae
40
Q

When should an oophrectomy be considered when performing a hysterectomy?

A
  • Decision to remove the ovaries will be largely dictated by whether the woman menopausal or not
  • In patients with dysmenorrhoea, the decision to perform an oophorectomy should be carefully considered because there are some common non-gynaecological causes of cyclical pain (e.g. IBS)
    • A 3-month trial of GnRH analogues to suppress ovarian function before surgery should be carried out to confirm that oophorectomy will alleviate the pain
41
Q

What are the main groups of young women you would consider an oophrectomy when doing an hysterectomy?

A
  • Debilitating premenstrual syndrome
  • Severe endometriosis
  • IMPORTANT: oophorectomy in young women is likely to require immediate systemic HRT
42
Q

Describe the pre-assessment of a hysterectomy

A
  • Patients usually present to pre-assessment clinic up to 2 weeks before the operation
  • All patients will have a:
    • FBC
    • Group and save
    • If > 50 years or known cardiac/renal/respiratory problems will have:
      • U&E
      • LFTs
      • Creatinine
      • CXR
      • ECG
  • Risk of thromboembolism will be assessed (plans for post-operative thromboprophylaxis can be made)
  • COCP should be STOPPED 4 weeks before the operation and alternative contraception should be used
  • HRT should also be stopped
  • LMWH may be given if HRT is to be continued
  • All women should be mobilised early after surgery
  • All women should be given thromboembolic stockings (TEDS) and kept hydrated
  • LMWH is given based on the risk assessment
43
Q

Describe thromboprophylaxis in a hysterectomy

A
  • LOW risk: surgery < 30 mins without risk factors
  • MODERATE risk
    • Use TEDS and LMWH
    • Surgery > 30 mins, high BMI, varicose veins, sepsis, immobility, comorbidity
  • HIGH risk
    • Use TEDS and LMWH for 5 days or until mobile
    • Cancer, prolonged surgery, previous thromboembolic event, thrombophilia or > 3 moderate risk factors
44
Q

What is a Pfannenstiel incision?

A
  • Transversely, two finger breaths above the pubic symphysis
  • Strong when repaired with low risk of herniation and dehiscence
  • Not very painful (limited to one or two dermatomes)
  • Cosmetically attractive (lower than the underwear line)
  • Cannot be easily extended or made larger
  • If extension is required, an inverted T incision is usually performed
  • Surgical access limited to pelvic organs
  • Used for uncomplicated gynaecological procedures
  • Below the arcuate line so there is NO posterior rectus sheath
45
Q

What is a midline incision?

A
  • Vertically from pubic symphysis up to umbilicus
  • Less strong: prone to herniation and dehiscence
  • Cosmetically unattractive
  • Can easily be extended to around the umbilicus up to the xiphisternum
  • Gives excellent surgical access
  • Useful if significant surgical difficulty is anticipated (e.g. adhesions, large fibroids, ovarian cysts)
  • More post operative pain
  • Increases risk of respiratory infection due to limited breathing and coughing effort
46
Q

Evaluate hysterectomy operations

A
  • Vaginal incisions have a low morbidity (almost no pain)
  • However, sometimes adhesion bands can form which interfere with intercourse
  • Laparoscopic surgery is also associated with low post-operative pain, better cosmetic outcomes and quicker discharge from hospital
47
Q

What are indications for a hysteroscopy?

A
  • Postmenopausal bleeding
  • Irregular menstruation (IMB, PCB)
  • Persistent heavy menstrual bleeding
  • Persistent discharge
  • Suspected uterine malformations
  • Suspected Asherman’s syndrome
  • Essure hysteroscopic sterilisation
  • Operating hysterectomy can also be used to resect fibroids, polyps and uterine septums
48
Q

What are complications of a hysteroscopy?

A
  • Perforation of the uterus
  • Cervical damage (if dilatation is needed)
  • Ascending infection (if infection present)
49
Q

What is a laparoscopy?

A
  • Allows visualisation of the peritoneal cavity
  • Involves insertion of a needle into a suitable puncture point in the umbilicus
  • Insufflation of the abdominal cavity allows larger instruments to be inserted
  • Operative laparoscopy can be done to perform ovarian cystectomy and oophorectomy and to treat endometriosis with cautery or laser
50
Q

What are indications for a laparoscopy?

A
  • Suspected ectopic pregnancy
  • Ovarian cyst accident and acute pelvic pain
  • Undiagnosed pelvic pain
  • Tubal patency testing
  • Sterilisation
51
Q

What are complications of a laparoscopy?

A
  • UNCOMMON
  • Damage to bowel and major blood vessels
  • Incisional hernia
52
Q

What are indications for cytoscopy?

A
  • Haematuria
  • Recurrent UTI
  • Sterile pyuria
  • Short history of irritative symptoms
  • Suspected bladder abnormality (e.g. diverticulum, stones, fistula)
  • Assessment of bladder neck
53
Q

What are complications of a cytoscopy?

A
  • UTI

- Bladder perforation (RARE)

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