Gynaecology Flashcards

1
Q

what are the 4 causes of ovarian cancer?

A
  • epithelial ovarian tumours
  • germ cell tumours
  • sex cord-stromal tumours
  • metastatic tumours
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2
Q

which is the most common type of ovarian cancer?

A

epithelial ovarian (85-90%)

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3
Q

features of an ovarian germ cell tumour

A
  • common in younger women (<35)
  • high survival rate
  • presents as a rapidly enlarging abdominal mass, can rupture or undergo torsion
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4
Q

where may tumours metastasise from to cause ovarian cancer?

A

breast, GI tract, haemopoietic system, uterus, cervix

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5
Q

risk factors of ovarian cancerr

A
  • increased age
  • lifestyle
  • talcum powder use pre-1975
  • history of infertility / use of fertility drugs (clomifene)
  • nulliparous women (never given birth)
  • early menarche/ late menopause
  • FH
  • HRT
  • endometriosis
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6
Q

where is the gene mutation located in patients with familial ovarian cancer?

A

BRCA 1 and 2

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7
Q

epidemiology of ovarian cancer

A

1/5 most common cancer in women

incidence rate increases with age, peaks around 70-80

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8
Q

clinical presentation of ovarian cancer

A
  • majority present late (stage III or IV)
  • insidious onset
  • IBS- like symptoms
  • abdominal discomfort, distention, bloating
  • urinary frequency
  • dyspepsia
  • fatigue
  • weight loss
  • pelvic or abdominal mass associated pain
  • abnormal uterine bleeding
  • ascites
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9
Q

differential diagnosis of ovarian cancer

A
  • benign ovarian tumour/ cyst
  • uterine or tubal mass
  • endometriosis
  • bowel mass
  • primary peritoneal carcinoma
  • secondary carcinoma
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10
Q

diagnostic tests and results in ovarian cancer

A
  • clinically- symptoms+age= likely
  • Ca125- tumour marker
  • USS + CT pelvis and abdo
  • CXR- pleural effusion/ lung mets
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11
Q

staging of ovarian cancer

A

1- limited to ovaries

2- involves one or both ovaries with pelvic extension and/or implants

3- involves one or both ovaries with microscopically confirmed peritoneal implants outside pelvis

4- one or both ovaries with distant mets

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12
Q

treatment of ovarian cancer

A
  • total abdominal hysterectomy and bilateral salpingo-oopherectomy (lymphadenectomy may be required also)
  • chemotherapy for III/IV after surgery
  • radiotherapy can be used in early disease
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13
Q

what is endometrial cancer?

A

cancer of the endometrium that arises from the lining of the uterus and is an oestrogen dependent tumour

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14
Q

risk factors for endometrial cancer

A
  • prolonged exposure to unopposed oestrogen
  • nulliparous
  • late menopause
  • obesity
  • endometrial hyperplasia
  • HNPCC
  • PCOS
  • diabetes
  • tamoxifen
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15
Q

what are the 2 types of andenocarcinoma’s seen in endometrial cancer?

A

type 1- oestrogen- dependent endometioid

type 2- oestrogen- independent non-endometrioid

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16
Q

epidemiology of endometrial cancer

A

90% of women are over 50 %

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17
Q

clinical presentation of endometrial cancer

A
  • early sign- post menopausal/ abnormal uterine bleeding

- heavy/ irregular periods in pre-menopausal women

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18
Q

diagnosis of endometrial cancer

A
  • clinical examination usually normal
  • Transvaginal US scan (looking for endometrial thickness >4mm)
  • endometrial pippelle biopsy if thickness >4mm
  • hysteroscopy
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19
Q

treatment of endometrial cancer

A

total abdominal/ laparoscopic hysterectomy with bilateral salpingo-oopherectomy (with possible lymphadenopathy depending on stage)

  • post op chemo
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20
Q

what causes cervical cancer?

A

persistent infection with human papillomavirus (HPV)

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21
Q

in cervical cancer, what is CIN?

A

CIN= Cervical Intraepithelial Neoplasia (also known as cervical dysplasia)

abnormal growth of cells on the surface of the cervix that could lead to cervical cancer

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22
Q

what are the 3 grades of CIN?

A

CIN I= lower basal 1/3 of cervical epithelium

CIN II= affects <2/3 of cervical epithelium

CIN III= affects >2/3 of full thickness of epithelium

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23
Q

who is screened for cervical cancer?

A

25-49- every 3 years

50-65- every 5 years

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24
Q

what is dyskaryosis?

A

dyskaryosis= abnormal nucleus and refers to the abnormal epithelial cell which may be found in cervical sample.

graded from low to high based on degree of abnormality

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25
Q

what tests and management plan are used for a borderline/ mild dyskaryosis?

A

test for HPV

negative= back to routine

positive= colposcopy

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26
Q

what tests and management plan are used for a moderate dyskaryosis?

A

urgent colposcopy within 2 weeks

consistent with CIN grade ii

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27
Q

what tests and management plan are used for a severe dyskaryosis or a suspected invasive cancer?

A

urgent colposcopy within 2 weeks, consistent with CIN III

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28
Q

what is the management plan if an inadequate cervical smear is provided?

A

repeat smear

if consistently inadequate, then colposcopy

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29
Q

risk factors for cervical cancer

A
  • persistence of HPV (high risk- HPV 16 and 18)
  • early intercourse (under 16)
  • multiple sexual partners
  • smoking
  • lower social class
  • immunosuppression (HIV, post-transplant)
  • COCP (combined oral contraceptive)
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30
Q

what are the 3 most common primary tumours seen in cervical cancer?

A
  • bulky, ectocervical tumour (fills upper vagina)
  • invasive, bulky tumour that can fill lower pelvis
  • destructive, invasive tumour that erodes tissues, causing ulceration and excavation with infected, necrotic cavities

70%= squamous cell

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31
Q

most common ages cervical cancer is seen in

A

25-34

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32
Q

clinical presentation of cervical cancer

A
  • abnormal vaginal bleeding (post coital)
  • vaginal discharge
  • post-micturition bleeding
  • vaginal discomfort/ urinary symptoms
  • haematuria
  • polyuria
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33
Q

differential diagnosis of cervical cancer

A
  • cervicitis
  • dysfunctional uterine bleeding
  • PID
  • endometrial cancer
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34
Q

diagnosis of cervical cancer

A
  • colposcopy/ cystoscopy- looking for irregular cervical surface
  • punch biopsy
  • bimanual examination

PET for staging

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35
Q

how is cervical cancer treated?

A

surgery- local excision (in a mild disease presentation) or full hysterectomy

chemotherapy- cisplatin

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36
Q

how is cervical cancer managed in pregnant women?

A

treatment delayed until a viable fetus can be delivered

in serious cases, therapeutic abortion may be necessary

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37
Q

aetiology of vulval cancer

A
  • Vulval intreepithelial neoplasia (HPV)
  • lichen sclerosis
  • squamous (90%)
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38
Q

symptoms of vulval cancer

A
  • vulvar itching
  • persistent ‘lump’
  • post-menopausal bleeding
  • pain passing urine
  • past history of VIN
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39
Q

diagnosis of vulval cancer

A

USS

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40
Q

treatment of vulval cancer

A

surgery and radiotherapy

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41
Q

what causes vaginal cancer?

A
  • HPV related
  • metastatic spread- cervical, uterine, vulval
  • pelvic radiotherapy
  • long term vaginal inflammation from pessaries

commonly squamous

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42
Q

presentation, treatment and prognosis of vaginal cancer

A

bleeding
radiotherapy
poor prognosis 58% 5 year survival

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43
Q

what can cause atrophic vaginitis?

A

caused by falling oestrogen levels

  • menopause
  • oohrectomy
  • anti-oestrogenic treatment- tamoxifen, aromatise inhibitors
  • radio/chemotherapy
  • post-partum
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44
Q

what changes of the mucosa and the vagina are seen in atrophic vaginitis?

A
  • thinner, drier, less elastic, fragile mucosa
  • inflamed vaginal epithelium
  • change in vaginal pH (can result in UTI’s)
  • pelvic laxity and STRESS INCONTINENCE
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45
Q

symptoms of atrophic vaginitis

A
  • vaginal dryness
  • burning/ itching of the vagina
  • dysparaeunia
  • vaginal discharge
  • post-coital and post-menopausal bleeding
  • urinary symptoms- polyuria, nocturia, dysuria, UTI’s, stress incontinence
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46
Q

clinical signs of atrophic vaginitis

A
  • reduced pubic hair
  • painful vaginal examination
  • lack of vaginal folds
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47
Q

differential diagnosis of atrophic vaginitis

A
  • genital infections
  • uncontrolled diabetes
  • local irritation due to soap etc
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48
Q

how is atrophic vaginitis diagnosed ?

A
  • diagnosis of exclusion

- TVS- transvaginal ultrasound to rule out pathology

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49
Q

treatment of atrophic vaginitis

A
  • vaginal lubricants
  • vaginal oestrogen
  • HRT
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50
Q

definition of atrophic vaginitis

A

thinning, drying and inflammation of the vaginal mucosa and epithelium that occurs due to a decrease in oestrogen

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51
Q

what are fibroids?

A

common benign tumours of the smooth muscle cells of the uterine myometrium

  • stimulated by oestrogen and progestogens
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52
Q

how are fibroids classified?

A

according to position in uterine wall

  • intramural- within endometrium
  • submucosal- growing into the uterine cavity
  • subserosal- growing outwards from uterus (can be uterine, cervical, intraligamentous, pedunculated subserous)
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53
Q

aetiology of fibroids

A

genetic

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54
Q

risk factors for fibroids

A
  • obesity
  • early menarche
  • afro-carribean
  • age 30-40
  • first degree relatives who had fibroids
  • COCP
  • pregnancy
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55
Q

clinical presentation of fibroids

A
  • 50% asymptomatic
  • prolonged, heavy periods
  • pelvic pain
  • recurrent miscarriage
  • sub-fertility
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56
Q

differential diagnosis of fibroids

A
  • dysfunctional uterine bleeding
  • endometrial polyps
  • pelvic inflammatory disease
  • ovarian tumour
  • pregnancy
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57
Q

diagnosis of fibroids

A
  • pregnancy tests
  • FBC- anaemia
  • TVUS
  • MRI
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58
Q

treatment of fibroids

A
  • tranexamic acid (antifibrinolytic agent)
  • GnRH agonists (goserelin)- shrinks fibroids
  • ulipristal acetate- progesterone receptor modulator
  • surgical- myomectomy
  • uterine artery embolisation
  • hysterectomy
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59
Q

what are the 3 types of ovarian cyst and which is most common?

A
  • functional (24%)
  • benign (70%)
  • malignant (6%)
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60
Q

what are 3 benign neoplastic causes of ovarian cysts?

A
  • benign epithelial neoplastic cysts
  • benign neoplastic cystic tumours of germ cell origin
  • benign neoplastic solid tumours
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61
Q

what are 3 benign fibrous causes of ovarian cysts?

A
  • adenofibroma
  • teratoma
  • brenner tumour
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62
Q

what is a brenner tumour?

A
  • rare ovarian tumour which displays in either a benign, borderline, proliferative or malignant variant
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63
Q

risk factors of ovarian cysts

A
  • obesity
  • tamoxifen therapy
  • early menarche
  • infertility
  • dermoid cysts- teratoma
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64
Q

when are ovarian cysts most commonly seen (epidemiology)

A

pre-menopausal women

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65
Q

clinical presentation of ovarian cysts

A
  • pain- dull ache, lower back pain, pain in lower abdo
  • irregular vaginal bleeding
  • swollen abdomen with palpable mass, dull to percussion
  • torsion, infarction or haemorrhage- severe pain
  • irregular vaginal bleeding
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66
Q

what findings on clinical examination would indicate the presence of an ovarian cyst?

A
  • swollen abdomen with palpable mass that is dull to percussion
  • ascites- malignancy
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67
Q

ovarian cysts- what can a hormone-secreting tumour cause?

A
  • virilisation
  • menstrual irregularities
  • post-menopausal bleeding
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68
Q

differential diagnosis of ovarian cysts

A
  • non-neoplastic functional cysts
  • PCOS
  • endometrioma
  • ovarial malignant tumour
  • bowel problems
  • PID
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69
Q

diagnostic tests and results in ovarian cysts

A
  • pregnancy test

FBC (infection, haemorrhage)

  • TVS
  • diagnostic laparoscopy
  • CA125- ovarian cancer tumour marker
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70
Q

what is the risk of malignancy index (RMI) used for and how is it scored?

A

RMI= suspected ovarian cancer

is a product of the USS score (below), menopausal status and serum Ca125 levels

USS score (1 point for each)

  • multi-ocular cysts
  • solid areas
  • metastases
  • ascites
  • bilateral lesions
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71
Q

what is a Rokitansky’s Protuberance and what does it indicate?

A

a solid protuberance from a mature dermoid cysts- indicates a teratoma

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72
Q

management of a small, medium and large ovarian cyst

A

small (<50mm) does not require follow up

medium (50-70mm) yearly US follow up

larger= MRI

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73
Q

what surgery is required in the treatment of ovarian cysts?

A

cystectomy

oopherectomy

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74
Q

how does ovarian torsion present?

A
  • sudden onset deep seated colicky pain
  • iliac fossa pain radiating to loin, groin or back
  • low grade fever
  • pain may start to improve after 24h- ovary dies at this point
  • vomiting and distress
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75
Q

what would an US show in a patient with ovarian torsion?

A

free fluid (oedema)- due to a cut off of venous supply

  • whirlpool sign- wrapping of vessels around a central axis
  • potential volvulus
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76
Q

how is ovarian torsion diagnosed and managed?

A

laparoscopy

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77
Q

what is Mittelschmerz?

A
  • mid cycle pain associated with ovulation
  • sharp onset
  • settles over 24-48 hours
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78
Q

what is endometriosis?

A

chronic, oestrogen dependent condition characterised by the growth of endometrial tissue in sites other than the uterine cavity

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79
Q

where is endometriosis most common?

A
  • pelvic cavity
  • uterosacral ligaments
  • pouch of Douglas
  • rectosigmoid colon
  • bladder
  • distal ureter
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80
Q

what is adenomyosis?

A

invasion of the endometrial tissue intro myometrium

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81
Q

aetiology of endometriosis

A
  • retrograde menstruation

- impaired immunity

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82
Q

risk factors for endometriosis

A
  • early menarche
  • late menopause
  • delayed childbearing
  • short menstrual cycles
  • obstruction to vaginal outflow
  • defects of uterus or fallopian tubes
  • genetic predisposition
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83
Q

give 2 protective factors for endometriosis

A
  • multiparity

- COCP

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84
Q

what is the triad of symptoms classically seen in endometriosis?

A
  • dysmenorrheoa
  • deep dyspareunia
  • cyclic/ chronic pelvic pain
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85
Q

other symptoms (other than the triad) in endometriosis

A
  • subfertility
  • dysuria
  • bloating
  • lethargy
  • constipation
  • lower back pain
86
Q

differential diagnosis of endometriosis

A
  • PID
  • ectopic pregnancy
  • torsion of ovarian cyst
  • appendicitis
  • primary dysmenorrhoea
  • IBS
  • uterine fibroids
87
Q

diagnostic test and results in endometriosis

A
  • laparoscopy w/ biopsy- gold standard
  • bimanual examination- finds a fixed, retroverted uterus
  • transvaginal ultrasound
  • MRI
88
Q

treatment of endometriosis

A
  • pain- NSAID’s
  • suppression of ovarian function for 6 months- COCP, medroxyprogesterone acetate, Goserelin (GnRH agonist)
  • surgery- laparoscopic excision or ablation, hysterectomy with salpingo-oopherectomy
89
Q

what is polycystic ovarian syndrome (PCOS)?

A

a syndrome of polycystic ovaries in association with systemic symptoms causing reproductive, metabolic and psychological disturbances

90
Q

what is the basic pathophysiology of PCOS?

A

excess androgens produced by theca cells of the ovaries due to:

  • hyperinsulinaemia
  • increased LH levels
91
Q

in PCOS, how are excess androgens caused by hyperinsulinaemia?

A
  • insulin resistance, weight gain leads to further insulin resistance
  • this leads to increased androgen production and reduced production of sex hormone-binding globulin (SHBG) in the liver
  • free testosterone is therefore raised
92
Q

clinical presentation of PCOS

A
  • oligomenorrheoa (<9 periods per year) and amenorrhoea
  • infertility and subfertility
  • signs of androgen production- acne, hirsutism, deepening voice, alopecia, male pattern balding, reduced breast size
  • obesity/ difficulty losing weight
  • psychological- mood swings, depression, anxiety, poor self esteem
  • sleep apnoea
  • acanthosis nigricans (due to insulin resistance)
93
Q

differential diagnosis of PCOS

A
  • thyroid disorder
  • hyperprolactinaemia
  • cushings syndrome
  • acromegaly
  • SE of medication
94
Q

what triad of clinical signs and symptoms must be seen to diagnose PCOS?

A
  • signs of excess androgen production
  • oligomenorrhoea/ amenorrhoea
  • cystic ovaries on US (12 or more on one ovary)
95
Q

other than the triad, what other tests and results are seen in PCOS?

A
  • testosterone normal/ raised
  • SHBD- low
  • LH levels- elevated
  • insulin resistance (impaired glucose tolerance)
  • normal prolactin
96
Q

what is the Rotterdam criteria in PCOS?

A

SHOP

  • string of pearls (cystic ovaries)
  • hyperandrogenism
  • oligomenorrhoea
  • prolactin normal
97
Q

treatment of PCOS

A

treat symptoms:
- hirsutism and acne- co-cyprindol

  • menstrual irregularity- COCP
  • insulin resistance= metformin
  • fertility- clomifene, metformin
98
Q

features of early menopause

A
  • irregular periods
  • vasomotor
  • vaginal dryness
  • poor concentration and fatigue
  • headaches
  • reduced libido
  • joint pain
99
Q

features of ongoing menoapuse

A
  • GU- frequency, urgency, nocturia, UTI;s
  • atrophic vaginitis
  • post-menopausal bleeding (PMB)
100
Q

features of late menopause

A
  • osteoporosis
  • dementia
  • cvd
101
Q

what is menopause?

A

permanent cessation of menstruation from loss of follicular activity

102
Q

symptoms and consequences of menopause

A
  • CV disease
  • vasomotor symptoms- hot flushes, night sweats, palpitations
  • urogenital problems- dysparaeunia, female sexual dysfunction, dryness, frequency, urgency, incontinence
  • osteoporosis
103
Q

what hormones are assessed in a patient with suspected menopause?

A
  • increased FSH

- anti-Mullerian hormone (direct measurement of ovarian reserve)

104
Q

treatment of menopause

A

HRT

  • treatment of hot flushes and night sweats- progesterone, clonidine, SSRI’s
  • osteoporosis- bisphosphonates, denossumab
105
Q

benefits of HRT

A
  • symptom management
  • osteoporosis prevention
  • colorectal cancer prevention
106
Q

risks of HRT

A
  • breast Ca if combined
  • endometrial cancer if oestrogen only
  • gallbladder disease
107
Q

differential diagnosis of bleeding

A
  • pregnancy- related- ectopic, hydatiform molar pregnancy, miscarriage
  • infection- chlamydia
  • vaginitis
  • fibroids
  • cervical ectropian
  • endometritis
  • cervical/ endometrial cancer
  • iatrogenic- tamoxifen, missed dose of OCP, post- smear
108
Q

postcoital bleeding differential diagnosis

A
  • infection
  • cervical/ endometrial polyps or cancer
  • cervical ectropion
  • trauma
109
Q

differential diagnosis of pelvic pain

A
  • ectopic
  • miscarriage
  • endometriosis
  • UTI
    PID
  • ovarian cyst rupture
110
Q

typical presentation of an ectopic pregnancy

A

female with a 6-8 wk amenorrhoea who presents with lower abdo pain, later develops vaginal bleeding

shoulder tip pain and cervical excitation may be seen

111
Q

typical presentation of pelvic inflammatory disease

A
  • pelvic pain
  • fever
  • deep dyspareunia
  • vaginal discharge
  • dysuria
  • menstrual irregularities
  • cervical excitation seen on examination
112
Q

typical presentation of ovarian torsion

A

sudden onset unilateral lower abdominal pain.

nausea, vomiting, unilateral tender adexal mass on examination

113
Q

typical presentation of miscarriage

A

vaginal bleeding and crampy lower abdominal pain following a period of amenorrhoea

114
Q

classic presentation of endometriosis

A

chronic pelvic pain
dysmenorrhoea
deep dyspareunia
subfertility

115
Q

classic presentation of an ovarian cyst

A

unilateral dull ache
torsion or rupture leads to severe abdo pain
large cyst- swelling or pressure effects on bladder

116
Q

classic presentation of a urogenital prolapse

A

seen in older women

sensation of pressure, heaviness and ‘bearing down’

urinary symptoms- incontinence, frequency, urgency

117
Q

what is the hypothalamic-pituitary axis?

A

GnRH- FSH- LH- oestrogen from ovaries

118
Q

describe the normal menstrual cycle

A

1-4- menstruation

5-13- proliferative phase

14-28- luteal/ secretory phase

119
Q

describe what happens between days 1-4 (menstruation) in the menstrual cycle

A
  • hormone support withdrawn
  • endometrial shed (<80ml blood loss)
  • some myometrial contractions can be painful
120
Q

describe what happens between days 5-13 (proliferative phase) in the menstrual cycle

A
  • GnRH stimulates FSH and LH
  • LH induces follicular growth- produces oestradiol and inhibin. this inhibits FSH with negative feedback
  • oestradiol continues to increase- endometrium thickens and reforms
  • positive feedback of LH causes ovulation
121
Q

describe what happens between days 14-28 (luteal/ secretory phase) in the menstrual cycle

A
  • follicle becomes the corpus luteum- produces more progesterone than oestradiol
  • results in increasing blood supply and enlargement of cells in endometrium
  • corpus luteum collapses near end if not fertilised. Oestrogen and progesterone levels fall
122
Q

what is premenstrual syndrome and what are the symptoms and management of it?

A

the emotional and physical symptoms that women experience prior to menstruation (in luteal phase)

  • symptoms- anxiety, stress, fatigue, mood swings
  • management- lifestyle, COCP and SSRI’s if severe
123
Q

what is the definition of menorrhagia?

A

excessive menstrual blood loss (>80ml) within a normal menstrual cycle, interfering with the womans physical, emotional and social quality of life

124
Q

causes of menorrhagia

A
  • majority have no pathology
  • 30% uterine fibroids
  • 10% polyps
  • PID, ovarian tumours, endometrial/ cervical malignancy
  • hypothyroidism
  • coagulation defects- Von-Willebrand or ITP
125
Q

how is menorrhagia assessed?

A
  • FBC, TSH, coag
  • transvaginal ultrasound- assesses endometrium for masses
  • if pt if >40 and the mass is >10mm, endometrial biopsy with hysteroscopy
126
Q

management of menorrhagia

A

medical
1st- IUS (mirena)
2nd- tranexamic acid, NSAID, COCP
3rd- progestogen

surgical:

  • endometrial ablation
  • resection of fibroids/ polyp
  • uterine artery embolisation
127
Q

what is intermenstrual bleeding?

A

vaginal bleeding at any times during the menstrual cycle other than during normal menstruation

128
Q

causes of intermenstrual bleeding

A
  • anovulatory cycles
  • fibrouds, polyps etc
  • if older woman, consider malignancy
129
Q

causes of post-coital bleeding

A
  • infection

- cervical ectropion, polyps or carcinoma

130
Q

what is amenorrhoea?

A

abscence of menstruation

131
Q

caues of amenorrhoea

A
  • primary- Turner’s syndrome, andorgen insensitivity syndrome, congenital malformations of genital tract, congential adrenal hyperplasia
  • secondary- is when previously normal mensturation ceases for >6 months
132
Q

what is oligomenorrhoea?

A

menstruation occurring every 35d- 6 months

133
Q

causes of oligomenorrhoea

A
  • physiological- pregnancy, menopause, lactation
  • hypothalamic hypogonadism
  • hyperprolactinaemia due to hypothyroidism
  • ovarian causes- PCOD, ovarian insufficiency, tumours
134
Q

investigations in Amenorrhoea

A
  • BhCG (pregnancy)
  • FSH/LH
  • Prolactin
  • TFT
  • Testosterone
135
Q

in amenorrhoea, what would a low FSH/ LH indicate?

A

hypothalamic pituitary ovarian axis problem

136
Q

in amenorrhoea, what would a high FSH/ LH indicate?

A

premature ovarian failure

137
Q

treatment of premature ovarian failure in amenorrhoea

A
  • cannot be reversed

- HRT to prevent oestrogen deficiency and therefore prevent osteoporosis

138
Q

in amenorrhoea, how is a malformation of the hypothalamic pituitary axis treated?

A
  • if mild- sufficient activity to stimulate enough oestrogen to produce an endometrium
  • severe- GnRH analogues
139
Q

if a woman who has amenorrhoea is asking for fertility, what would be provided?

A

clomifene

140
Q

what is Lichen Sclerosis?

A

chronic inflammatory dermatosis that affects the skin of the anogenital region in women or the glans penis and foreskin in men

141
Q

aetiology of Lichen Sclerosis

A

autoimmune induced

142
Q

clinical presentation of Lichen Sclerosis (in males and females)

A
  • white thickened patches which may have ecchymosis, hyperkeratosis or bullae
  • females- itchy, pain, perianal lesions, white lesions (figure 8 around vulvula and anus), shrinking of labia
  • men- soreness, painful erections, dysuria
143
Q

differential diagnosis of Lichen Sclerosis

A
  • child sexual abuse
  • vitiligo
  • scleroderma
  • lichen planus
144
Q

treatment of lichen sclerosis

A

topical steroids- clobetasol propionate

145
Q

what is an ectopic pregnancy and where do they commonly occur?

A

a pregnancy that occurs anywhere outside the uterus

  • 97% in fallopian tubes
  • 2-3% occur as interstitial ectopic pregnancies
146
Q

risk factors of an ectopic pregnancy

A

IVF, age, PID, previous ectopic, smoking, adhesions from infection, inflammation from endometriosis, previous tubal surgery

147
Q

clinical presentation of an ectopic pregnancy

A
abdominal/ pelvic pain
amenorrhoea (6-8 weeks)
vaginal bleed 
pelvic tenderness 
dizziness, fainting, syncope
rebound tenderness 

SHOULDER TIP PAIN

148
Q

differential diagnosis of an ectopic pregnancy

A
  • threatened miscarriage
  • appendicitis
  • bowel ischaemia
149
Q

diagnosis of an ectopic pregnancy

A
  • pregnancy test- no rapid decline of BhCG
  • transvaginal USS
  • empty uterus w/ positive pregnancy test
  • cervical excitation on pelvic exam
150
Q

treatment of an ectopic pregnancy

A
  • initial- FC, crossmatch, IV fluids

- if foetal heartbeat- salpingectomy/ salpingotomy

151
Q

what is pelvic inflammatory disease?

A
  • general term for infection of the upper female genital tract
152
Q

causes of PID

A
  • gonorrhoea + chlamydia
  • vaginal anaerobes
  • sti
  • pregnancy
  • miscarriage
  • uterine instrumentation
153
Q

risk factors for developing PID

A
  • young
  • new sexual partner/ multiple sexual partners
  • lack of barrier contraception
  • lower socio-economic group
  • IUD present
154
Q

clinical presentation of PID

A
  • bilateral lower abdominal pain
  • deep dyspareunia
  • abnormal vaginal bleeding
  • vaginal or cervical purulent discharge
  • abdo tenderness
  • fever
155
Q

presentation of acute salpingitis/ PID

A
  • fever, tachycardia
  • lower abdo tenderness
  • cervicitis
156
Q

differential diagnosis of PID

A
  • appendicitis

- ectopic pregnancy

157
Q

diagnosis of PID

A
  • pregnancy test
  • cervical swab
  • raised ESR and CRP
  • biopsy
  • USS
158
Q

treatment of clinically severe PID

A
  • ceftriaxone 500mg
  • doxycycline
  • metronidazole
159
Q

what is dysmenorrhoea?

Dysmennorhoea is associated with high levels of what?

A

painful menstruation associated with high prostaglandin levels in the endometrium due to contraction and uterine ischaemia

160
Q

primary and secondary causes of dysmenorrhoea?

A

primary- no organic cause

secondary- pelvic pathology- fibroids, adenomyosis, endometriosis, PID

161
Q

treatment of primary dysmenorrhoea

A

NSAIDS and COCP

162
Q

What is a genitourinary prolapse?

A

descent of one or more of the pelvic organs including the uterus, bladder, rectum small/ large bowel or vaginal vault

resulting in protrusion of the vaginal walls

163
Q

risk factors of genitourinary prolapse

A
increasing age
vaginal delivery 
increasing parity
high BMI 
spina bifida 
pelvic mass
menopause
164
Q

pathophysiology of GU prolapse

A

occurs when support structure (levator ani muscles and endopalvic fascia) is damaged- trauma etc

165
Q

clinical presentation of an anterior compartment GU collapse

A

urethrocele- prolapse of urethra into vagina

cystocele- prolapse of bladder into vagina

cystourethrocele- both of the above

166
Q

clinical presentation of a middle compartment GU collapse

A
  • uterine prolapse- descent of uterus into vagina
  • vaginal vault prolapse- descent of the vaginal vault post-hysterectomy
  • enterocele- herniation of pouch of Douglas into the vagina
167
Q

clinical presentation of a posterior compartment GU collapse

A

rectocele- prolapse of the rectum into the vagina

168
Q

stages of a genitourinary prolapse

A

0- no prolapse

1- more than 1cm above hymen

2- within 1cm proximal or distal to the plane of the hyman

3- more than 1cm below the plane of the hymen but protrudes no further than 2cm less than the total length of vagina

4- complete eversion of the vagina

169
Q

features of asymptomatic genitourinary prolapse

A

sensation of dragging down, pressure, fullness or heaviness

sensation of bulge

discomfort

spotting

IF ANTERIOR- incontinence, urgency, frequency

170
Q

diagnostic tests and results in a GU prolapse

A
  • history and examination- sims speculum
171
Q

treatment of a GU prolapse

A
  • conservative- aims to reduce intrabdominal pressure (lose weight, stop smoking, treat cough, stop constipation, pelvic floor exercises)
  • vaginal pessary insertion
  • surgery- hysterectomy, colporrhaphy
172
Q

what are the 2 types of incontinence?

A

urgency- overactive bladder (involuntary detrusor muscle bladder contractions)

stress- sphincter weakness (detrusor pressure > closing pressure of urethra)

173
Q

symptoms of an overactive bladder

A
urgency 
frequency 
nocturia 
'key in door'
ensuresis
174
Q

symptoms of stress incontinence (what brings it on?)

A

cough, laughing, lifting, exercise, movement

175
Q

causes of stress incontinence

A
  • menopause- low oestrogen results in weakening pelvic support
  • radiotherapy, congenital weakness, pelvic surgery
176
Q

‘simple assessments’ of incontinence

A
  • Dipstick/urinalysis – UTI check
  • MSU (Midstream urine sample for urinalysis below)
-FVC (frequency volume chart) (urine diary)
▪ Frequency and quantity of urination
▪ Frequency and quantity of leakage
▪ Fluid intake
▪ Diurnal variation
  • RU (residual urine measurement)
    ▪ In and out catheter
    ▪ USS
177
Q

what is the ePAQ questionarre?

A

determines impact on life of variety of issues to determine management plan (of incontinence)

  • Urinary- pain / voiding / overactive bladder / stress
    incontinence / QoL
  • Vaginal- Pain / capacity / prolapse / QoL
  • Bowel- IBS / constipation/ continence / QoL
  • Sexual- Urinary / bowel / vaginal / dyspareunia / overall
    sex life
178
Q

what are the treatment options of incontinence?

A
  • lifestyle- reduce caffiene, weight loss, smoking cessation

- containment- bladder bypass (catheters), vaginal support devices

179
Q

treatment of stress incontinence

A
  • pelvic floor training
  • SNRI- duloxetine
  • surgery
180
Q

treatment of an overactive bladder

A
  • bladder drills
  • anticholinergics
  • antimuscarinics- solifenacin, oxybutynin
  • adrenergic agonist- mirabegron
  • botox
181
Q

what is a rectocele?

A

prolapse of the lower posterior wall of the vagina, involving the anterior wall of the rectum

182
Q

symptoms of a rectocele

A
  • constipation

- difficulty with defecation

183
Q

how is a rectocele managed?

A

posterior repair

184
Q

what is a cystocele?

A

prolapse fo the anterior vaginal wall, involving the bladder

  • usually associated with prolapse of the urethra, in this case it is referred to as a cysto-urethrocele prolapse
185
Q

how does a cystocele/ cysto-urethrocele present clinically?

A
  • urinary urgency and frequency
  • incomplete bladder emptying
  • urinary retention/ reduced flow
186
Q

how is a cystocele managed?

A

anterior repair

187
Q

what is a vesicovaginal fistula?

A

opening from the vaginal tract into the urinary tract

188
Q

aetiology of a vesicovaginal fistula

A
  • trauma
  • abdo hysterectomy
  • vaginal hysterectomy
  • vaginal/ bladder biopsy
  • radiation therapy
189
Q

how does a vesicovaginal fistula present clinically?

A

continuous incontience presenting after recent pelvic trauma/ surgery

190
Q

what is a hydatidiform mole?

A

growth of an abnormal fertilised egg

191
Q

how does a hydatidiform mole present clinically?

A
  • irregular 1st trimester vaginal bleeding
  • large uterus for dates
  • exaggerated pregnancy symptoms- hyperemesis, hyperthyroidism, pre-eclampsia
192
Q

how does a complete hydatidiform mole present on an USS?

A

‘snowstorm appearance’

193
Q

how is a hydatidiform mole managed (complete and partial)?

A

complete- surgical evacuation, give oxytocin to reduce haemorrhage risk

partial- medical evacuation if small enough

194
Q

what is Adenomyosis?

A

presence of endometrial glands and stroma within the myometrium

195
Q

what symptoms would a patient with adenomyosis present with clinically and how would this present on examination?

A

symptoms- dysmennorhoea, menorrhagia, dyspareunia, cyclical pelvic pain

usually presents after pregnancy
O/E- enlarged ‘boggy’ uterus

196
Q

how is adenomyosis diagnosed?

A

histopathology

197
Q

how is a patient with adenomyosis managed?

A

continuous OCP’s- for symptoms

  • only curative Tx is a hysterectomy
198
Q

what is androgen insensitivity syndrome?

A

mutation in androgen receptor gene results in resistance to androgens in target tissues- so body does not respond to male sex hormones

  • X linked recessive pattern-
  • patient is 46XY but appears female
199
Q

in a patient with complete androgen insensitivity syndrome, how do their genitalia present?

A
  • female external genitalia
  • short blind-ending vagina
  • absent uterus and fallopian tubes
  • normal breast development
  • sparse pubic and axillary hair
  • undescended testes
200
Q

how does a patient with partial androgen insensitivity syndrome present clinically?

A

‘under-masculinisation’

ambiguous genitalia

201
Q

when and how does mild androgen insensitivity syndrome present?

A

will not present until puberty

high pitched voice and gynaecomastia

202
Q

how is androgen insensitivity syndrome managed

A

gonadectomy and HRT

203
Q

what is dysfunctional (abnormal) uterine bleeding?

A

irregular uterine bleeding that occurs in the absence of recognisable pelvic pathology or pregnancy

204
Q

aetiology of dysfunctional uterine bleeding

A
  • PCOS
  • endometriosis
  • polyps/ fibroids
  • STD
  • Warfarin, spironolactone, OCP
205
Q

what is an endometrial polyp and what % of these are malignant?

A

focal overgrowth of the endometrium

1% are malignant

206
Q

how are endometrial polyps treated?

A

resection during hysteroscopy

send for histological assessment

207
Q

what is a prolactinoma and how are they classified?

A

commonest pituitary tumour seen in pregnancy

macroprolactinoma= >1cm

microprolactinoma= <1cm

208
Q

outside of pregnancy, diagnosis of a prolactinoma is based on serum prolactin level, why is this not the case in pregnancy?

how are they diagnosed in pregnancy instead?

A

during pregnancy, serum prolactin levels rise significantly anyways so this is not useful

imaging- CT etc

209
Q

clinical features of a prolactinoma?

A
  • amenorrhoea
  • galactorrhoea
  • headache
  • visual field defects- bitemporal hemianopia
  • diabetes insipidus
210
Q

what medications that are normally used to manage a proclactinoma should be stopped in a pregnant lady?

A

dopamine receptor agonists- cabergoline and bromocriptine (bromocriptine can be restarted if there is a fear the tumour is expanding)

211
Q

how are prolactinomas in pregnancy managed?

A

surgery- but delay until after delivery unless critical