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PHASE 3A > WOMENS HEALTH - urogynae, gynae > Flashcards

WOMENS HEALTH - urogynae, gynae Flashcards

1
Q

what are the 2 main types of breast cancer?

A
  1. ductal carcinoma in situ (DCIS)
  2. lobular carcinoma in situ (LCIS)

(inflammatory breast cancer is rare type)

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2
Q

is breast cancer the most common cancer type?

A

yes - it overtook lung

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3
Q

describe the aetiology of breast cancer

A

mix of genetic and environmental factors - BRCA1 and BRCA2

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4
Q

modifiable and non-modifiable RFs for breast cancer?

A

modifiable - obesity, alcohol

nonmodifiable - late first childbirth, heritability, early menarche (<12), late menopause (>55)

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5
Q

why are early menarche and late menopause RFs for breast cancer?

A

both increase the breast tissue’s exposure to oestrogen over a woman’s lifetime > oestrogen promotes the proliferation of breast cells

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6
Q

how is breast cancer screened?

A

mammogram every 3 YEARS to women aged 50-70

if women are high risk e.g. genetic, can get annual screening from age 30

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7
Q

signs and symptoms of breast cancer (general)

A
  • asymptomatic!
  • painless lump (hard, irregular, fixed)
  • nipple inversion
  • peau d’orange
  • nipple discharge
  • skin tethering
  • Paget’s disease of the breast
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8
Q

signs/symptoms that breast cancer has become metastatic?

A

fractures, seizures

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9
Q

3 key signs/symptoms of inflammatory breast cancer

A
  1. peau d’orange
  2. inflamed breast
  3. nipple inversion
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10
Q

how is breast cancer investigated?

A

triple assessment

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11
Q

outline the triple assessment for breast cancer

A
  1. clinical assessment
  2. imaging assessment (mammography, USS or MRI)
    if abnormal, go onto…
  3. biopsy assessment (fine needle aspiration or core biopsy)

scored 1-5 in each (1 normal, 5 malignant)

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12
Q

when is MRI scanning useful for breast cancer in the imaging assessment?

A
  • when patient has breast implants/in young patients with more dense breasts
  • when patient has higher risk e.g. strong fhx
  • to further assess size/features of tumour
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13
Q

what might a mammogram scan show if the patient has BC?

A

calcification, irregular mass

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14
Q

which chromosomes are BRCA1 and BRCA2 on, respectively?

A

brca1 = chromosome 17

brca2 = chromosome 13

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15
Q

what is triple-negative breast cancer?

A

the breast cancer cells do not express any cancer receptors (e.g. ER, PR, HER2) that treatments can target and act upon

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16
Q

common locations for breast cancer metastasis

A

REMEMBER 2Ls and 2Bs

L - lungs
L - liver
B - bones
B - brain

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17
Q

what are the 3 types of breast cancer receptors?

A
  1. oestrogen receptors (ER)
  2. progesterone receptors (PR)
  3. human epidermal growth factor (HER2)
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18
Q

what system is used to stage breast cancer?

A

TNM - tumour (T), nodes (N), metastasis (M)

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19
Q

what is the nottingham prognostic index?

A

a tool to predict survival after breast cancer surgery

uses tumour size, lymph node status and tumour grade

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20
Q

which breast cancer type tends to be grade 3?

A

triple negative

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21
Q

surgical management options for breast cancer and their indications

A
  1. breast conservation + radio therapy
    indications = small tumour relative to breast size
  2. mastectomy
    indications = personal pref, large tumour relative to breast size, more than 1 cancer in same breast
  3. axillary surgery (full or limited)
    indications = if spread into axillary system
  4. reconstructive surgery
    indications = offered to all pts having mastectomy
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22
Q

common complication of axillary surgery?

A

lymphoedema

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23
Q

non-surgical management options for breast cancer

A
  1. chemo
  2. hormone treatment - tamoxifen if PREmenopausal and aromatase inhibitors e.g. anastrozole if POSTmenopausal
  3. targeted tx e.g. trastuzumab, pertuzumab
  4. chemoprevention (for high risk women) - tamoxifen for pre and anastrozole for postmenopause
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24
Q

when is chemotherapy indicated in breast cancer?

A

in HIGH RISK disease…
- young age
- high grade
- node +ve
- tumour size
- ER-ve, HER-2+ve
- Ki67 positive

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25
Q

which breast cancer is hormone treatment indicated for?

A

for patients with oestrogen-receptor (ER) positive breast cancer

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26
Q

which breast cancer is targeted tx indicated for?

A

HER2+ve

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27
Q

which breast cancer is associated with good prognosis?

A

DCIS - ductal carcinoma in situ

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28
Q

define atrophic vaginitis

A

thinning, drying and inflammation of the vaginal walls

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29
Q

what causes atrophic vaginitis?

A

often lack of oestrogen

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30
Q

when does atrophic vaginitis often occur?

A

around/after the menopause

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31
Q

how does atrophic vaginitis present?

A

often a woman during/after her menopause
- dryness
- burning
- discharge
- itching
- burning with urination
- urgency, frequency
- recurrent UTIs
- postcoital bleeding
- dyspareunia

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32
Q

investigations for atrophic vaginitis

A
  • pelvic examination
  • vulva, vaginal and cervical exam
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33
Q

management of atrophic vaginitis

A
  1. topical vaginal oestrogen e.g. ovestin, gynest (cream) or vagifem (tablet)

if topical oestrogen contraindicated, can use vaginal moisturisers/lubricants

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34
Q

when is topical oestrogen contraindicated?

A

hx of breast cancer

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35
Q

what are the types of cervical cancer? which is most common?

A
  • 80% are squamous cell carcinoma
  • next most common is adenocarcinoma
  • v rare other types e.g. small cell
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36
Q

what system is used to stage cervical cancer? what are the stages?

A

the international federation of gynae & obstetrics (FIGO) system
stage 1 - confined to cervix
stage 2 - invades uterus or upper 2/3 of vagina
stage 3 - invades pelvic wall or lower 1/3 of vagina
stage 4 - invades bladder, rectum or beyond pelvis

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37
Q

which women are most commonly affected by cervical cancer?

A

younger, peaks in reproductive
years

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38
Q

what causes cervical cancer?

A

strongly associated with human papillomavirus (HPV)
types 16 and 18 - responsible for 70% of cervical cancer

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39
Q

RFs for cervical cancer (think of 3 categories)

A

think of the RFs in terms of:
1. increased risk of catching HPV
2. non-engagement with screening
3. others

increased risk of HPV:
- early sexual activity
- increased no. sexual partners
- sexual partners who’ve had more partners
- not using condoms

others:
- smoking
- HIV
- combined contraceptive pill use for >5y
- increased no. of full-term pregnancies
- family hx
- exposure to diethylstilbesterol during foetal development

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40
Q

pathophysiology of cervical cancer

A

HPV produces proteins (E6 and E7) that inhibit tumour suppressive genes

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41
Q

signs and symptoms of cervical cancer

A

(may be detected during cervical smears in asymptomatic women)

  • abnormal vaginal bleeding: intermenstrual, postcoital, postmenopausal
  • vaginal discharge
  • pelvic pain
  • dyspareunia
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42
Q

investigations for cervical cancer

A

may be found during routine screening

  1. cervical smear screen - speculum and swabs
    if abnormal (e.g. ulceration, inflammation, bleeding, visible tumour)&raquo_space; urgent cancer referral for…
  2. colposcopy
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43
Q

what is the grading system diagnosed in colposcopy? what are the grades?

A

Cervical Intraepithelial Neoplasia (CIN)
grades the level of dysplasia in the cells of the cervix
1. CIN I - mild dysplasia, affecting 1/3 thickness of the epithelial layer. likely to return to normal
2. CIN II - moderate dysplasia, affecting 2/3 thickness of the epithelial layer. likely to progress to cancer if untreated
3. CIN III - severe dysplasia, v likely to progress to cancer

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44
Q

what is cervical intraepithelial neoplasia (CIN) III also known as?

A

cervical carcinoma in situ

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45
Q

cervical cancer management
a) CIN and early stage 1A
b) stage 1B-2A
c) stage 2B-4A
d) stage 4B

A

a) LLETZ or cone biopsy (esp good for women who want to preserve fertility)

b) radical hysterectomy, removal of local lymph nodes with chemo and radio

c) chemo and radio

d) may involve combo of surgery, radio, chemo and palliative

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46
Q

preventative management of cervical cancer

A

HPV vaccine
- given to boys and girls before they’re sexually active
- helps prevent contraction and spread
- vaccine = gardasil

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47
Q

when is cervical screening offered?

A

every 3 years aged 25-49

every 5 years aged 50-64

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48
Q

describe the steps in a cervical smear test

A
  1. speculum inserted, cells collected
  2. sample tested for high-risk HPV (if negative, cells not further examined, smear deemed negative)
  3. if HPV positive, cells examined under microscope for precancerous change (dyskaryosis) - called cytology
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49
Q

summarise the management of the 4 different smear test results

A
  1. inadequate sample - repeat in >3m
  2. HPV negative - continue routine screening
  3. HPV positive with normal cytology - repeat HPV test after 12m (if happens twice in a row, refer to cytology)
  4. HPV positive with abnormal cytology - refer for colposcopy
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50
Q

what does colposcopy involve when investigating cervical cancer? what stains are used?

A
  • acetic acid stain: abnormal cells go white
  • schiller’s iodine test: healthy cells go brown, abnormal won’t stain
  • can get tissue sample with punch biopsy
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51
Q

what is adenomyosis?

A

abnormal growth of endometrial tissue into the myometrium (uterus lining grows into wall and muscle)

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52
Q

which women typically suffer from adenomyosis?

A

women at the end of their reproductive years who have had multiple children (multiparous)

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53
Q

signs (uterus on palpation) and symptoms of adenomyosis

A
  1. menorrhagia
  2. dysmenorrhoea (pain before and/or during menstruation)
  3. dyspareunia
  4. boggy enlarged uterus on palpation
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54
Q

investigations for adenomyosis
a) initial
b) 1st line
c) diagnostic

A
  1. pelvic exam - tender, BOGGY, ENLARGED
  2. 1st line = transvaginal US
  3. diagnostic/gold std = biopsy after hysterectomy
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55
Q

how do you tell between somebody presenting with adenomyosis and endometriosis?

A

both present with painful periods, but adenomyosis also presents with heavy bleeding

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56
Q

management for adenomyosis
1. first line
2. for symptoms
3. definitive

A
  1. 1st line = contraception e.g. mirena coil
  2. symptomatic tx - mefenamic acid, tranexamic acid, GnRH agonists
  3. definitive tx = hysterectomy
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57
Q

complications of adenomyosis during pregnancy

A

infertility, miscarriage, preterm baby, PPH

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58
Q

define endometriosis
where is commonly affected?

A

chronic, inflammatory disease characterised by the growth of ectopic endometrial tissue OUTSIDE of the uterus

commonly in ovaries, broad ligaments and fallopian tubes

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59
Q

what are chocolate cysts?

A

found in endometriosis - endometriomas (fluid-filled cysts) in the ovaries

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60
Q

what % of women suffer with endometriosis?

A

10%

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61
Q

although the exact cause of endometriosis is unknown, suggest some theories

A
  1. genetics
  2. endometrial lining flows backwards during menstruation through fallopian tubes > pelvis and peritoneum (retrograde menstruation)
  3. embryonic cells meant to become endometrial tissue remain outside of uterus during foetal development
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62
Q

signs and symptoms of endometriosis

A
  • cyclical pelvic/abdo pain
  • secondary dysmenorrhoea (often starts days before bleeding)
  • deep dyspareunia
  • subfertility
  • cyclical non-gynae sx with periods eg.. dysuria, haematuria, urgency, dyschezia (painful bowel movements)
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63
Q

investigations for endometriosis

A
  1. pelvic exam - tender, reduced cervical mobility, palpable cysts, potentially visible endometrial tissue on speculum
  2. 1st line = TVUSS
  3. gold std/diagnostic = laparoscopic exploration and biopsy
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64
Q

management pathway for endometriosis

A
  1. NSAIDs/paracetemol
    if ineffective…
  2. hormonal therapies e.g. COCP, depo-provera injection, implant, mirena coil, GnRH agonists
    OR
  3. if fertility needs to be improved, surgery e.g. laparoscopic to excise/ablate tissue
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65
Q

define
a) perimenopause
b) menopause
c) premature menopause

A

a) time from the first experience of symptoms until bleeding has stopped for a year

b) retrospective diagnosis confirmed when >12m of amenorrhoea in the absence of hormonal contraceptives in women aged 49-52

c) cessation of periods before 40 y/o

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66
Q

what is the mechanism of menopause?

A
  1. ovaries depleted of follicles over time (as born with finite pool of primordial follicles)
  2. so decline of oestrogen production
  3. lack of oestrogen > lack of negative feedback on pituitary gland > rise of FSH and LH
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67
Q

short-term symptoms of menopause (4 categories)

A
  1. vasomotor
    - hot flushes
    - sweats (night)
    - palpitations
    - headaches
  2. psych
    - irritability
    - low mood
    - lethargy
    - forgetfulness
    - libido
  3. urogenital (atrophy due to lack of oestrogen)
    - vaginal dryness
    - dyspareunia
    - frequency, urgency
  4. skin
    - dry skin and hair
    - brittle nails
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68
Q

long-term consequences of menopause

A
  1. osteoporosis
  2. CVD e.g. myocardial infarction, angina, stroke
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69
Q

how is menopause diagnosed?

A

mainly clinical diagnosis but can confirm with lab tests

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70
Q

what will laboratory tests show in menopause?

A
  • high FSH
  • low oestrogen and progesterone
  • low inhibin
  • normal testosterone and prolactin
  • normal TSH
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71
Q

treatment options and what they are for in menopause
a) acute symptomatic
b) HRT

A

a)
- SSRIs or clonidine for flushes
- topical oestrogen gel for atrophy

b)
- improves sx within 4w
- protects CVD and osteoporosis
- oestrogen (estradiol) and progesterone (medroxyprogesterone) options
- transdermal where possible

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72
Q

which women are indicated for oestrogen-only HRT tx for menopause? why?

A

those that don’t have a uterus

progesterone protects against endometrial cancer, so give combined to those with uterus

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73
Q

what HRT therapy should be given if:
a) LMP was <year ago
b) LMP was >year ago

A

a) sequential combined
b) continuous combined

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74
Q

when should you advise women that they may stop taking contraception if they are:
a) >50
b) <50

A

a) can stop taking 12m after periods ended
b) can stop taking 24m after periods ended

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75
Q

why is transdermal HRT preferred to oral?

A

oral carries a VTE risk

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76
Q

what is the underlying pathology of:
a) urge incontinence
b) stress incontinence

A

a) overactivity of the detrusor muscle of the bladder (aka overactive bladder)

b) weakness of the pelvic floor and sphincter muscles allowing urine to leak at times of increased pressure on the bladder

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77
Q

typical presentation of:
a) urge incontinence
b) stress incontinence

A

a) suddenly feeling urge to pass urine, rushing to bathroom, getting there too late, v conscious about having access to a toilet

b) urinary leakage when laughing, coughing or surprised

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78
Q

what is overflow incontinence?

A

chronic urinary retention due to obstruction to the outflow of urine

results in overflow of urine and incontinence without the urge to pass urine

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79
Q

RFs for urinary incontinence (8)

A
  1. increased age
  2. postmenopause
  3. increased BMI
  4. prev pregnancies and vaginal deliveries
  5. pelvic organ prolapse
  6. pelvic floor surgery
  7. neuro conditions e.g. MS
  8. cognitive impairment/dementia
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80
Q

how can you assess urinary incontinence through examination?

A
  1. assess pelvic tone
  2. examine for pelvic organ prolapse/atrophic vaginitis/pelvic masses
  3. ask patient to cough and watch for leakage from the urethra
  4. bimanual exam - ask woman to squeeze against examining fingers (assesses strength of pelvic muscle contractions)
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81
Q

investigation options for urinary incontinence (4)

A
  1. bladder diary
  2. urine dipstick (rule out infection, haematuria)
  3. post-void residual bladder volume (check for incomplete emptying)
  4. urodynamic testing (for urge incontinence not responding to tx)
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82
Q

management options for stress incontinence (lifestyle, 1st and 2nd line)

A
  1. lifestyle - avoid caffeine, diuretics, overfilling bladder, weight loss
  2. 1st line = pelvic floor exercises for at least 3m
  3. 2nd line (if exercises not working >3m) - either surgery or duloxetine if surgery less preferred
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83
Q

management options for urge incontinence (1st, 2nd, 3rd line)

A

1st line - bladder retraining (gradually increasing time between voiding) for at least 6w

2nd line - anticholinergics e.g. oxybutynin

3rd line - invasive procedures e.g. botulinum toxin type A injection

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84
Q

side effects of anticholinergics e.g. oxybutynin used in the management of urge incontinence

A

anticholinergic effects e.g. dry mouth, dry eyes, urinary retention, constipation and postural hypotension

also cognitive decline, memory probs and worsening of dementia

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85
Q

alternative medical treatment to anticholinergics for urge incontinence

A

mirabegron

but is contraindicated in uncontrolled hypertension

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86
Q

what is a uterine/uterovaginal prolapse?

A

loss of anatomical support for the uterus, causing herniation of the uterus into the vaginal canal

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87
Q

what 3 conditions are encompassed by the term pelvic organ prolapse (POP)?

A

cystocele (bladder), rectocele (rectum) and cystourethrocele (uterus)

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88
Q

risk factors for uterine prolapse (6)

A
  1. vaginal delivery
  2. older age
  3. high BMI
  4. prev surgery for prolapse
  5. gynae surgery e.g. cancer
  6. heavy lifting
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89
Q

signs and symptoms of uterine prolapse

A

depends on severity/stage

  • sensation of vaginal bulging
  • pelvic pressure
  • urinary sx e.g. frequency, incontinence, incomplete emptyinh
  • defecatory dysfunction
  • dyspareunia

LATE STAGE - palpable protruding cervix

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90
Q

how is a uterine prolapse diagnosed?

A

clinically - diagnosis normally made by vaginal exam during resting and standing

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91
Q

other investigations for a uterine prolapse e.g. to confirm diagnosis/check for complications

A
  • bimanual examination
  • speculum
  • bladder diary
  • MSU dip (higher risk of infection)
  • postvoid residual vol scan (prolapse can result in retention)
  • questionnaire
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92
Q

management of asymptomatic uterine prolapse

A
  • observation
  • pelvic floor exercises
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93
Q

management of symptomatic uterine prolapse

A

1st line = pessary (shelf, ring, gellhorn)

surgery if indicated

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94
Q

when is surgery indicated for uterine prolapse?

A

symptomatic e.g. dyspareunia, obstruction, discomfort despite exercises/pessary

severe prolapse e.g. outside vagina, ulcerated

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95
Q

what is the most common endometrial cancer?

A

adenocarcinoma

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96
Q

what stimulates endometrial cancer cell growth? so when does this cancer commonly present?

A

oestrogen! it’s an oestrogen-dependent cancer

so commonly presents in post-menopause when woman has been exposed to oestrogen for their whole lives

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97
Q

risk factors for endometrial cancer

A

all in relation to UNOPPOSED OESTROGEN (oestrogen without progesterone)

  1. increased age
  2. obesity (adipose tissue source of oestrogen)
  3. early menarche
  4. late menopause
  5. oestrogen-only HRT
  6. no/few pregnancies
  7. PCOS (lack of ovulation - during ovulation corpus luteum produces progesterone)
  8. tamoxifen
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98
Q

which hereditary condition is a risk factor for endometrial cancer?

A

hereditary nonpolyposis colorectal cancer (HNPCC) or lynch syndrome

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99
Q

what key presentation should immediately make you suspicious of endometrial cancer?

A

any woman with postmenopausal bleeding

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100
Q

besides postmenopausal bleeding, how can endometrial cancer present?

A
  • postcoital bleeding
  • intermenstrual bleeding
  • menorrhagia
  • abnormal discharge
  • haematuria
  • anaemia
  • raised platelets

PAIN NOT COMMON - signifies extensive disease

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101
Q

what is the referral criteria for endometrial cancer for a 2-week wait urgent referral?

A

postmenopausal bleeding (>12m after last menstrual period)

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102
Q

1st line and other investigations for endometrial cancer

A
  1. 1st line = TVUS (for endometrial thickness)
  2. pipelle biopsy (highly sensitive and less invasive than…)
  3. hysteroscopy with endometrial biopsy
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103
Q

what endometrial thickness is normal on TVUS and indicates low risk for endometrial cancer?

A

<4mm

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104
Q

stages of endometrial cancer

A
  1. confined to uterus
  2. invades cervix
  3. invadies ovaries, fallopian tubes, vagina or lymph nodes
  4. invades bladder, rectum or beyond pelvis
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105
Q

surgical management for endometrial cancer (stages 1-2)

A

total abdominal hysterectomy with bilateral salpingo-oophorectomy (TAH and BSO)

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106
Q

surgical management for endometrial cancer (stages 3+)

A

radical hysterectomy (removes pelvic lymph nodes, surrounding tissues and top of vagina

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107
Q

what option can be offered to manage endometrial cancer in frail old women not suitable for surgery?

A

progesterone therapy

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108
Q

what are fibroids?
what are the 3 different types?

A

benign endometrial neoplasms (uterine leiomyomas) aka abnormal growths made of myometrium

  1. submucosal - beneath endometrium
  2. intramural - within muscular wall
  3. subserosal - beneath peritoneum
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109
Q

what are fibroids an important differential for?

A

secondary dysmenorrhoea

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110
Q

risk factors for fibroids

A
  1. obesity
  2. family hx (genetic component)
  3. smoking
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111
Q

what makes fibroids grow?

A

they are oestrogen responsive!

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112
Q

signs and symptoms of fibroids

A
  • often asymptomatic!
  • menorrhagia = most frequent presenting symptom
  • dysmenorrhoea
  • abnormal bleeding e.g. postmenopause
  • deep dyspareunia
  • bloating/feeling full
  • bowel and bladder sx (if large enough to press)
  • enlarged uterus
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113
Q

investigations for fibroids (1st line, diagnostic etc)

A
  1. 1st line = hysteroscopy
  2. diagnostic = TVUSS
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114
Q

management for asymptomatic fibroids

A

no treatment, regular FU

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115
Q

management for symptomatic fibroids that are:
a) <3cm
b) >3cm

A

a)
1st line = MIRENA COIL
symptom management = NSAIDs, tranexamic acid
other options = COCP, cyclical oral progesterone
surgical = ablation, resection during hysteroscopy

b) same medical options as above but will need referral to gynae
surgical = uterine artery embolisation, myomectomy, hysterectomy

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116
Q

what medication can be used prior to fibroid surgery?

A

GnRH agonists - mimics menopause and shrinks fibroids

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117
Q

what is a dangerous complication of fibroids in pregnant women? how does it present?

A

RED DEGENERATION - fibroids increase v quickly in size due to increased oestrogen of pregnancy, outgrow blood supply in 2nd/3rd trimester and die

present with fever, abdominal pain, vomiting

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118
Q

other complications of fibroids (5)

A
  1. heavy bleeding w iron deficiency
  2. reduced fertility
  3. miscarriage/prem labour/obstructive delivery
  4. constipation
  5. UTIs
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119
Q

what is bacterial vaginosis? what bacterial changes is it characterised by?

A

a dysbiosis of the vagina

overgrowth of anaerobic organisms (e.g. Gardnerella vaginalis) and loss of healthy acid-producing lactobacilli

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120
Q

what is the pH in BV?

A

loses normal acidity, pH is >4.5

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121
Q

risk factors for BV?

A
  1. sex life - active, multiple male partners, female partners, recent change in partner, receptive oral sex, unwashed toys, not using condoms
  2. excessive cleaning e.g. douching, using cleaning products
  3. copper coil
  4. smoking
  5. poor genital hygiene
  6. ethnicity (more common in black women)
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122
Q

how does BV present?

A
  • 50% asymptomatic!
  • primary sx = fishy-smelling, thin, grey-white discharge
  • NOT associated with itching/soreness
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123
Q

Amsel’s criteria for BV (3 of the following 4)

A
  1. thin, white homogenous discharge
  2. clue cells on microscopy
  3. pH >4.5
  4. positive whiff test (addition of potassium hydroxide = fish smell)
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124
Q

investigations for BV

A

rarely need speculum unless high risk of STI/pregnant/pre or post termination

  1. vaginal pH swab (>4.5)
  2. either HVS or self-taken low swab with microscopy (clue cells)
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125
Q

management of BV if:
a) asymptomatic
b) symptomatic
c) pregnant

A

a) tx not required

b) oral metronidazole 5-7 days

c) if asymptomatic, discuss with obstetrician. if symptomatic can have oral metronidazole (but not high dose regimen) or topical tx e.g. metronidazole/clindamycin

126
Q

what advice needs to be given when prescribing metronidazole?

A

don’t drink alcohol

127
Q

what is a hydatidiform mole and what is it caused by?
what is a
a) complete mole
b) partial mole

A

a type of tumour that grows like a pregnancy inside the uterus, also known as a molar pregnancy. caused by a non-viable fertilised egg implanting in the uterus

a) two sperm cells fertilise an ovum containing no genetic material > no foetal material forms

b) two sperm cells fertilise a normal ovum at the same time > new cell has 3 chromosome sets > some foetal material may develop but cannot survive

128
Q

which stage of pregnancy does a hydatidiform mole present?

A

early stages - first 3m

129
Q

RFs for a hydatidiform mole

A
  1. <18 or <35
  2. asian/mexican background
  3. diet low in carotene (vit A)
  4. previous molar pregnancy/gestational trophoblastic tumour
130
Q

signs and symptoms of a hydatidiform mole

A

sx similar to pregnancy:
- periods stop
- hormonal changes of pregnancy

sx indicating molar vs normal:
- more severe morning sickness
- vaginal bleeding
- increased enlargement of uterus
- abnormally high hCG
- thyrotoxicosis

131
Q

investigations and findings for a hydatidiform mole (3)

A
  1. bloods - hCG very high
  2. pelvic USS - ‘snowstorm’ appearance
  3. definitive = histology of mole after evacuation
132
Q

management of a hydatidiform mole

A
  1. surgery - evacuation of uterus and products sent for histological exam
  2. FU
    - referred to gestational trophoblastic disease centre
    - hCG monitored until normal
133
Q

define androgen insensitivity syndrome. what kind of inheritance is it carried by?

A

X-LINKED RECESSIVE condition

end-organ resistance to testosterone causing genotypically male children (XY) to have an external female phenotype

134
Q

briefly outline the pathophysiology of androgen insensitivity syndrome

A
  1. cells unable to respond to testosterone due to lack of androgen receptors
  2. extra testosterone turns into oestrogen
  3. typical male sexual characteristics don’t develop
  4. external female genitalia and breast tissue develops
  5. BUT internal female genitalia prevented from growing by anti-mullerian hormone
135
Q

describe the uterus, testes and vagina in a patient with androgen insensitivity syndrome

A

no uterus, undescended testes, short vagina

136
Q

what mutation causes androgen insensitivity syndrome?

A

mutation in the androgen receptor gene on the X chromosome

137
Q

signs and symptoms of androgen insensitivity syndrome if presenting in:
a) infancy
b) puberty

A

a) inguinal hernias containing testes

b) primary amenorrhoea, little/no axillary or pubic hair, facial hair, male type muscle development

138
Q

investigations for androgen insensitivity syndrome

A
  1. hormone blood tests - abnormal
  2. examination - will show short vagina
  3. buccal smear/chromosomal analysis - will show 46XY genotype
139
Q

hormonal blood test results in androgen insensitivity syndrome
a) LH
b) FSH
c) testosterone
d) oestrogen

A

a) raised
b) normal/raised
c) normal/raised (for a male)
d) raised (for a male)

140
Q

surgical and non-surgical management options for androgen insensitivity syndrome

A

surgical:
- bilateral orchiectomy
- vaginal dilation/surgery (create adequate length)

non-surgical:
- oestrogen replacement
- psychosocial help

141
Q

what is a complication for pts with androgen insensitivity syndrome?

A

testicular cancer (due to undescended testes)

142
Q

what are the 5 criteria that need to be met for expectant management of an ectopic pregnancy?

A
  1. unruptured embryo
  2. asymptomatic
  3. <35mm size
  4. no foetal heartbeat
  5. B-hCG level <1000 and declining
143
Q

what is lichen sclerosus? what is it characterised by?

A

a chronic inflammatory (possibly autoimmune) condition characterised by patches of shiny, ‘porcelain-white’ skin

incurable

144
Q

RFs for lichen sclerosus (5)

A
  1. other autoimmune diseases e.g. type 1 diabetes, alopecia, hypothyroid, vitiligo
  2. older age
  3. increased BMI
  4. smoking
  5. preceding infection/skin trauma
145
Q

what is a typical exam stem scenario testing lichen sclerosus?

A

a woman aged 45-60 complaining of vulval itching and skin changes

146
Q

signs and symptoms of lichen sclerosus

A
  • shiny, porcelain-white patches of skin (labia, perineum and perianal skin - NOT inside vagina)
  • other skin changes = tight, thin, slightly raised, papules/plaques
  • itching
  • soreness (poss worse at night)
  • superficial dyspreunia
  • erosions/fissures
  • Koebner phenomenon (sx made worse by friction to skin e.g. tight underwear, urinary incontinence and scratching)
147
Q

investigations for lichen sclerosus

A

usually clinical - hx and exam

IF doubt can do vulval biopsy

148
Q

lichen planus vs lichen sclerosus

A

lichen planus - lesions INSIDE vagina
lichen schlerosus - lesions OUTSIDE (labia, perineum, perianal skin)

149
Q

management for lichen sclerosus including FU

A

cannot be cured but sx can be managed!

  1. 1st line = potent topical steroids e.g. clobetasol propionate 0.05% (dermovate) - use every day initially then twice weekly (but go back to daily if flare until good control)
  2. emollients regularly used
  3. FU every 3-6 months with gynae/derm
150
Q

what does lichen sclerosus increase the risk of in 5% of women?

A

developing squamous cell carcinoma of the vulva

151
Q

why does tamoxifen help treat breast cancer but is a risk factor for endometrial cancer?

A

it acts as an oestrogen-receptor antagonist in the breast tissue but an oestrogen agonist in endometrial tissue

152
Q

what may endometrial hyperplasia present with?

A

intermenstrual bleeding, post-menopausal bleeding, menorrhagia or irregular bleeding

153
Q

what is a common cause of secondary amenorrhoea in very athletic women?

A

hypothalamic hypogonadism

154
Q

what medication for urinary incontinence should not be used in the elderly population? why? what are some safer alternatives?

A
  • oxybutynin
  • increased risk of falls
  • solifenacin, tolterodine, mirabegron
155
Q

what is ovarian hyperstimulation syndrome? what may it present with?

A

a complication arising during IVF caused by using hCG in the maturation of follicles

presents with lower abdo discomfort, nausea, vomiting, and abdo distension

156
Q

what is Asherman’s syndrome?

A

when adhesions (called synechiae) of endometrium form within the uterus, causing damage

157
Q

what causes Asherman’s syndrome?

A

most often pregnancy-related dilatation and curettage procedure - used for abortion, miscarriage, retained placenta (creates scar tissue)

158
Q

signs and symptoms of Asherman’s syndrome

A

typically presents following recent dilatation and curettage/uterine surgery with…
- SECONDARY AMENORRHOEA
- significantly lighter periods
- dysmenorrhoea
- fertility probs

159
Q

investigations for Asherman’s syndrome

A

often found incidentally during hysteroscopy

gold std = hysteroscopy

other options = hysterosalpingography, sonohysterography, MRI

160
Q

treatment for Asherman’s syndrome

A

surgical - dissecting adhesions during hysteroscopy

161
Q

complication of Asherman’s syndrome

A

infertility

162
Q

what is a genital tract fistula?

A

an abnormal opening between the vagina and other nearby organs e.g. bladder or rectum

163
Q

causes of a genital tract fistula (5)

A
  1. PROLONGED/OBSTRUCTIVE CHILDBIRTH
  2. pelvic surgery
  3. radiation tx
  4. Crohn’s/UC
  5. retained foreign material e.g. pessary
164
Q

signs and symptoms of a genital tract fistula

A

classic = women who had prolonged/obstructive childbirth presenting with urinary/faecal leakage

other:
- abnormal vaginal discharge
- foul odour in urine/discharge
- recurrent infections e.g. UTI
- bleeding
- passage of gas from urethra during urination

165
Q

investigations for a genital tract fistula (5) - especially if presenting with incontinence

A
  1. pelvic exam
  2. DYE TEST - insert dye into bladder/rectum and check for leakage into vagina (if incontinence)
  3. imaging e.g. USS
  4. colonoscopy
  5. cystourethroscopy
166
Q

management of small and large genital tract fistulas

A

small - may heal on its own with use of bladder catheter

large - surgical

167
Q

a congenital abnormality regarding the female organs (upper vagina, uterus and fallopian tubes) is related to which structure in the foetus?

A

the mullerian ducts (paramesonephric ducts)

168
Q

embryologically, where do the upper vagina, cervix, uterus and fallopian tubes develop from?

A

the paramesonephric ducts (mullerian ducts)

169
Q

which hormone in the male foetus suppresses the growth of female reproductive organs?

A

anti-Mullerian hormone

170
Q

a) what is a bicornuate uterus?
b) how does it present?
c) how is it diagnosed?

A

a) a congenital malformation of the uterus, resulting in two cavities instead of one (“heart-shaped”)

b) adverse pregnancy outcome e.g. miscarriage, premature birth, malpresentation

c) pelvic USS

171
Q

a) what is an imperforate hymen?
b) how and when does it often present?

A

a) congenital malformation where the hymen at the vaginal entrance is fully formed, so there is no opening

b) often discovered at menstrual age - will have cyclical pelvic pain and cramping WITHOUT BLEEDING (primary dysmenorrhoea)

172
Q

how is an imperforate hymen diagnosed? what will be seen?

A

clinical examination - a bulging blue membrane will be seen

173
Q

tx of an imperforate hymen

A

surgical incision

174
Q

complication of untreated imperforate hymen

A

retrograde menstruation (which can lead to endometriosis)

175
Q

what is a transverse vaginal septae? what are the types?

A

congenital malformation resulting in a septum (wall) forming transversely across the vagina

can be perforate (with hole/s) or imperforate (completely sealed)

176
Q

presentation of
a) perforate transverse vaginal sepate
b) imperforate transverse vaginal septae

A

a) girl may be able to menstruate but will have difficulty with tampon use/sex

b) similar to imperforate hymen - primary amenorrhoea

177
Q

complications of transverse vaginal septae

A

infertility and pregnancy related complications

178
Q

how are transverse vaginal septae diagnosed?

A

examination, USS or MRI

179
Q

tx and tx complications for transverse vaginal septae

A

tx = surgical correction
cx = vaginal stenosis, recurrence of septae

180
Q

what is vaginal…
a) hypoplasia
b) agenesis

what are they both due to?

A

a) abnormally small vagina
b) absent vagina

due to failure of Mullerian ducts to properly develop

181
Q

vaginal hypoplasia/agenesis may also be associated with absent…

A

uterus and cervix

182
Q

what is usually unaffected in vaginal hypoplasia/agenesis?

A

the ovaries&raquo_space; normal female sex hormones

183
Q

management of vaginal hypoplasia/agenesis

A

either use of vaginal dilator over long period (create adequate size) OR vaginal surgery

184
Q

what are endometrial polyps? how big are they?

A

intrauterine endometrial neoplasms that attach to the inner wall and grow inwards

vary from mm to several cm

185
Q

when are endometrial polyps common?

A

end of reproductive age

186
Q

aetiology of polyps

A

hormones - they grow in response to oestrogen (oestrogen sensitive)

187
Q

RFs for polyps

A
  1. older age
  2. HTN
  3. obesity
  4. hyperestrogenism
  5. PCOS
  6. late menopause
  7. chronic liver disease
188
Q

which drug therapy is a RF for polyp formation?

A

tamoxifen (breast cancer drug therapy)

189
Q

presentation of endometrial polyps

A

may be asymptomatic!

if symptomatic…
- abnormal bleeding
- postcoital spotting
- less common = infertility

190
Q

investigation of choice for polyps in…
a) women of reproductive age
b) infertile patients with suspected polyps

A

a) TVUSS
b) hysteroscopy

191
Q

treatment of asymptomatic polyps

A

no tx needed

192
Q

treatment of polyps if symptomatic/pt has risk factors for endometrial cancer

A

hysteroscopic polypectomy

193
Q

complication of polyps in a v small number of women (0-12%)

A

malignant transformation

194
Q

how do you know what the first day of a woman’s period is?

A

first day of bleeding = first day of period (FIXED POINT)

195
Q

describe the hypothalamus-pituitary-ovary axis, including the negative feedback cycles

A
  1. hypothalamus - releases GnRH (gonadotropin-releasing hormone)
  2. stimulates pituitary to release LH and FSH
  3. LH and FSH stimulates release of oestrogen and progesterone from the ovaries
  4. oestrogen and progesterone have negative feedback effect on both the pituitary (LH/FSH) and hypothalamus (GnRH)
196
Q

4 aims of the menstrual cycle

A
  1. develop dominant follicle
  2. prepare endometrium for implantation of embryo
  3. release an oocyte
  4. maintain endometrium while waiting for fertilisation

then starts again

197
Q

phases of the menstrual cycle

A
  1. follicular phase
  2. luteal phase
198
Q

when is the follicular phase? which days of the cycle?

A

= from start of menstruation to moment of ovulation

the FIRST 14 days of the cycle (1-14)

199
Q

what are the steps of the follicular phase?
describe the levels of LH/FSH/oestrogen/progesterone at each point

A
  1. day 1, all hormones at base level, LOW oestrogen and progesterone
  2. then LH begins to rise
  3. rising LH stimulates developing follicles
  4. as follicles grow, they release oestrogen
  5. oestrogen initially has -ve feedback on pituitary, so LH and FSH reduce
  6. one dominant follicle continues to develop
  7. oestrogen then suddenly gives +ve feedback, LH SPIKES
  8. this spike causes dominant follicle to release ovum from ovary (=OVULATION!)
    end of follicular phase
200
Q

define a:
a) oocyte
b) follicle
c) ovum

A

a) immature cell which will go on to become an ovum
b) oocyte surrounded by granulosa cells
c) unfertilised egg

201
Q

when does ovulation ALWAYS occur? so when would ovulation occur in:
a) a 28 day cycle
b) a 30 day cycle
c) a 40 day cycle

A

always occurs 14 days before the end of the menstrual cycle
so
a) day 14 in a 28 day cycle
b) day 16 in a 30 day cycle
c) day 26 in a 40 day cycle

202
Q

when is the luteal phase? which days?

A

from the moment of ovulation to the start of menstruation
final 14 days of the cycle

203
Q

describe the steps of the luteal phase

A
  1. dominant follicle collapses and forms corpus luteum
  2. corpus luteum secretes progesterone and v small amount of oestrogen
  3. corpus luteum has fixed life of 14 days
  4. unless maintained by pregnancy (by release of hCG), corpus luteum regresses to corpus albicans and stops producing progesterone and oestrogen
  5. falling progestrone = shedding endometrium = BLEEDING
  6. menstruation starts on day 1 of cycle
  7. negative feedback from oestrogen and progesterone ceases, so LH and FSH rise again > cycle restarts
204
Q

there are always X days between ovulation and menstruation

A

14 days (bc corpus luteum has fixed life of 14d)

205
Q

what happens to the endometrium in the menstrual phase? under the influence of what hormone?

A

days 1-5
FALLING LEVELS OF PROGESTERONE
shedding of endometrium, superficial and middle layers separate from basal layer

206
Q

what happens to the endometrium in the proliferative phase? under the influence of what hormone?

A

following menstruation - endometrium GROWS under influence of rising OESTROGEN

207
Q

what happens to the endometrium in the proliferative phase? under the influence of what hormone?

A

following menstruation - endometrium GROWS under influence of rising OESTROGEN

208
Q

what happens to the endometrium in the secretory phase? under the influence of what hormone?

A
  • following ovulation
  • PROGESTERONE predominates
  • proliferation stops and REMODELLING starts
  • to prepare for implantation e.g. development of glands, spiral arterioles, endometrial cells produce and store glycogen
209
Q

when do progesterone levels peak in the menstrual cycle? e.g. in a 28 day cycle

A

peak 7 days AFTER OVULATION

and remember ovulation is always 14 days before the end of the cycle
so in a 28 day cycle, 14+7 = day 21

210
Q

what hormones should be checked when assessing a woman’s fertility? when?

A

LH and FSH - day 2-5
peak progesterone - 7 days before start of next period (or 7 days after ovulation)

211
Q

what day should peak progesterone be measured when investigating fertility in a patient who’s cycle is
a) 28 days
b) 35 days
c) 41 days

A

minus 7!!!

a) 21
b) 28
c) 34

212
Q

what diagnosis is likely in a girl presenting with late menarche and HIGH FSH and LH?

A

Turner’s syndrome - gonadal dysgenesis

213
Q

what is the most common type of ovarian cancer?

A

epithelial cell tumour - most common is serous carcinoma

214
Q

FIGO staging of ovarian cancer (4)

A
  1. confined to ovary
  2. spread past ovary but inside pelvis
  3. spread past pelvis but inside abdo
  4. spread outside abdo (distant metastasis)
215
Q

what prognosis does ovarian cancer generally carry? why?

A

poor prognosis - often diagnosed late

216
Q

peak age of incidence of ovarian cancer

A

60 years old

217
Q

ovarian cancer…
a) risk factors (4)
b) protective factors (3)

A

a)
- BRCA1/BRCA2
- increased no. of ovulations e.g. early-onset periods, late menopause, no pregnancies
- obesity
- smoking

b)
- COCP
- breastfeeding
- pregnancy

218
Q

signs and symptoms of ovarian cancer

A

can be non-specific!
- abdominal bloating
- early satiety, loss of appetite
- pelvic pain
- HIP/GROIN PAIN (specific, ovarian mass pressing on obturator nerve)
- urinary sx e.g. frequency, urgency
- weight loss
- abdo/pelvic mass
- ascites

219
Q

ovarian cancer referral criteria for 2-week wait (3)

A
  1. ascites
  2. pelvic mass
  3. abdominal mass
220
Q

initial investigations for ovarian cancer - what result would indicate further testing and what further test would be done?

A

first = CA125 blood test
if raised (>35 IU/ml)&raquo_space; URGENT ultrasound of abdo and pelvis

221
Q

what is the tumour marker for epithelial cell ovarian cancer? but what else may it be raised in?

A

CA125
not v specific - also raised in endometriosis, menstruation, fibroids, adenomyosis etc

222
Q

following bloods and USS, what further investigations are done for establishing a diagnosis of ovarian cancer?

A
  1. CT
  2. diagnostic laparotomy
223
Q

what is the risk of malignancy index (RMI)? what does it take into account?

A

scoring system that estimates the risk of an ovarian cancer being malignant
takes into account
1. menopausal status
2. USS findings
3. CA125 level

224
Q

management of ovarian cancer

A

usually mix of surgery and platinum-based chemo

225
Q

what are functional ovarian cysts? who are they common in?

A

cysts (fluid-filled sacs) in the ovaries relating to the fluctuating hormones in menstruation
v common in premenopausal women
majority are benign

226
Q

what are the 2 types of functional ovarian cysts? which is most common?

A
  1. follicular cyst (most common)
  2. corpus luteum cyst
227
Q

in which women are ovarian cysts rarer and more worrying? what may they indicate?

A

postmenopausal women - concerning for malignancy

228
Q

pathophysiology of functional cysts (follicular and corpus luteum)

A

follicular - fail to rupture and release egg, cyst persists
corpus luteum - fails to break down, instead fills w fluid

229
Q

when are corpus luteum cysts most common?

A

early pregnancy

230
Q

ovarian cysts (non-functional): pathophysiology of
a) serous cystadenoma
b) mucinous cystadenoma
c) endometrioma
d) dermoid cysts/germ cell tumours

A

a) and b) benign tumour of epithelial cells
c) lumps of endometrial tissue
d) benign ovarian tumour deriving from germ cells (teratomas)

231
Q

which complication are dermoid cysts/germ cell tumours associated with?

A

ovarian torsion

232
Q

signs and symptoms of ovarian cysts (most are ___?)

A

most are asymptomatic and found incidentally
if symptomatic:
- pelvic pain
- bloating
- fullness in abdomen
- palpable pelvic mass (esp if v large)

233
Q

which type of ovarian cyst can grow huge and is most likely to be palpable?

A

mucinous cystadenoma

234
Q

what should first be assessed when a patient presents with a possible ovarian cyst?

A

whether cyst could be malignant…
thorough history (features of malignancy e.g. bloating, pain, urinary sx, ascites, lymphadenopathy) and assess for RFs e.g. age, post-menopause, family hx

235
Q

imaging choice for investigating ovarian cyst
next steps if cyst is…
a) <5cm
b) >5cm

A

PELVIC USS
a) premenopausal women with cyst <5cm do NOT need further investigating
b) further investigation required: measure CA125

236
Q

indications for checking CA125 in a patient with an ovarian cyst (2)

A
  1. cyst >5cm on pelvic USS
  2. postmenopausal women
237
Q

what investigation should be done for complex (multi-focal) ovarian cysts?

A

cyst needs to be biopsied to assess for malignancy

238
Q

indications for a 2-week wait gynae cancer referral in a woman with ovarian cyst/s

A
  1. raised CA125
  2. complex cysts
239
Q

management of simple ovarian cysts in premenopausal women
a) <5cm
b) 5-7cm
c) >7cm

A

a) will resolve within 3 menstrual cycles, don’t need FU
b) routine referral to gynae and yearly USS
c) consider MRI/surgical evaluation

240
Q

management of ovarian cysts in postmenopausal women

A
  1. correlation with CA125 result and referral to gynae
  2. simple cysts <5cm with normal CA125 may be monitored with USS every 4-6m
241
Q

management of persistent/enlarging cysts

A

surgical intervention - laparoscopy, ovarian cystectomy, potential oophorectomy

242
Q

what 3 complications should be considered in a women with an ovarian cyst presenting with acute pain?

A
  1. ovarian torsion
  2. haemorrhage into cyst
  3. rupture, with bleeding into peritoneum
243
Q

Meig’s syndrome
a) what is it and what triad does it present with?
b) who is it typical in?
c) management

A

a) benign ovarian tumour presenting with triad of ovarian fibroma, pleural effusion and ascites - look out for women presenting with pleural effusion and ovarian mass
b) older women
c) cyst removal

244
Q

what is ovarian torsion?

A

when the ovary twists in relation to the surrounding connective tissue, fallopian tube and blood supply (the adnexa)

245
Q

which two groups are at a higher risk of ovarian torsion?

A
  1. pregnant women
  2. younger girls before menarche
246
Q

why are younger girls pre-menarche more at risk of ovarian torsion?

A

they have longer infundibulopelvic ligaments that can twist more easily

247
Q

risk factors for ovarian torsion (3)

A
  1. having an ovarian cyst/tumour
  2. pregnancy
  3. premenarche
248
Q

presentation of ovarian torsion

A

main presenting feature = SUDDEN ONSET SEVERE UNILATERAL PELVIC PAIN

  • pain is constant
  • getting progressively worse
  • associated N&V
  • localised tenderness on examination
249
Q

investigations for ovarian torsion:
a) first-line
b) definitive

A

a) pelvis USS (transvaginal)
b) laparoscopic surgery

250
Q

what might you see on TVUSS in ovarian torsion? (3)

A
  • “whirlpool sign”
  • free fluid in pelvis
  • oedema of ovary
251
Q

surgical management options for ovarian torsion

A

either
1. untwist ovary (detorsion)
2. oophorectomy

decision made during surgery on visual inspection

252
Q

what is pelvic inflammatory disease (PID)?

A

infection/inflammation of the female pelvic organs (uterus, fallopian tubes, ovaries and surrounding peritoneum)

253
Q

what is the most common causative organism of PID? what are some other potential organisms?

A

most common = Chlamydia trachomatis

others = Neisseria gonorrhoea, Mycoplasma genitalium, Mycoplasma hominis

254
Q

signs and symptoms of PID (6)
what is a classic sign on examination?

A
  1. lower abdo pain
  2. fever
  3. deep dyspareunia
  4. dysuria
  5. menstrual irregularities
  6. discharge

on exam - cervical excitation (makes pt jump when cervix moved side to side)

255
Q

investigations for PID (4)

A
  1. pregnancy test
  2. high vaginal swab HSV
  3. screen for chlamydia and gonorrhoea (NAAT and culture for chlamydia, MSU for men and HSV for females for gonorrhoea)
  4. urinalysis
256
Q

management of PID

A

ORAL OFLOXACIN + ORAL METRONIDAZOLE

or

IM ceftriaxone + oral doxycycline + oral metronidazole

(consider removal of IUD)

257
Q

a) name a classic complication of PID
b) what is it characterised by?

A

a) perihepatitis (Fitz-Hugh Curtis syndrome)
b) fever, PID, RUQ pain

258
Q

other complications of PID (2)

A
  1. infertility
  2. ectopic pregnancy
259
Q

what is PCOS? what is it characterised by? (5)

A
  • a common condition causing metabolic and reproductive problems
  • characterised by multiple ovarian cysts, infertility, oligomenorrhoea, hyperandrogenism and insulin resistance
260
Q

what age-group does PCOS present in?

A

reproductive age

261
Q

brief pathophysiology of PCOS

A
  1. excessive production of oestrogen by ovaries
  2. impaired metabolism, disrupted hormonal feedback mechanisms
  3. consistent high oestrogen levels > irregular menstrual cycles and anovulation (need LH spike in menstrual cycle to release ovum from dominant follicle - don’t get this if -ve feedback from oestrogen all the time)
  4. no corpus luteum
  5. prolonged exposure to unopposed oestrogen (as corpus luteum produces progesterone)
262
Q

KEY features of PCOS (5)

A
  1. oligomenorrhoea or amenorrhoea
  2. infertility
  3. obesity
  4. hirsutism
  5. acne
263
Q

OTHER features/complications of PCOS

A
  1. insulin resistance/diabetes
  2. acanthosis nigricans
  3. CVD
  4. hypercholesteremia
  5. endometrial hyperplasia/cancer
  6. obstructive sleep apnoea
  7. depression and anxiety
  8. sexual problems
264
Q

what are the Rotterdam criteria for PCOS? how many do you need?

A

have to have 2 of…
1. oligoovulation or anovulation (presents as irregular/absent periods)
2. hyperandrogenism (presents with hirsutism and acne)
3. polycystic ovaries on USS

265
Q

first line and diagnostic investigations for PCOS

A

first line = bloods (sex hormones, insulin, prolactin, TSH)

GS = TVUSS

266
Q

what findings would be found when doing blood tests in a patient with PCOS…
a) testosterone
b) LH and FSH (inc ratio)
c) oestrogen
d) insulin
e) prolactin
f) TSH

A

a) testosterone normal/mildly raised
b) raised LH and raised LH:FSH ratio
c) oestrogen normal/raised
d) insulin raised
e) prolactin may be mildly elevated
f) normal (excludes thyroid probs)

267
Q

what sign will be seen on TVUSS in PCOS? what is diagnostic?

A

“string of pearls”

diagnostic = either 12 or more developing follicles in each ovary OR ovarian volume >10cm3

268
Q

general/lifestyle management options for PCOS

A
  1. weight reduction
  2. exercise
  3. smoking cessation
  4. antihypertensive meds if needed
  5. for contraception - COCP (regulate cycle and induce monthly bleed)
269
Q

management options of endometrial cancer risk in PCOS

A
  • mirena coil (for continuous protection)
  • COCP (to also induce a bleed if needed/wanted)
270
Q

management of hirsutism/acne in PCOS (first and second line)

A

first line = COCP (co-cyprinidiol)

if not working then topical eflornithine
weight loss also helps

271
Q

management of infertility in PCOS (first line and other options)

A

non pharm: weight loss
pharm: first line = clomifene
second line = metformin/combo of both

272
Q

what will a patient with PCOS need to be screened for if they become pregnant?

A

gestational diabetes

273
Q

what is nephrolithiasis?

A

the presence of crystalline stones (calculus) within the kidneys/ureter

274
Q

what is the most common cause of urinary obstruction?

A

ureteric stones

275
Q

what are kidney stones most commonly made of?

A

calcium oxalate

276
Q

RFs for kidney stones (5)

A
  1. dehydration
  2. high salt intake
  3. white
  4. male
  5. obesity
277
Q

what are the 3 common sites where calculi get stuck in the urinary system?

A
  1. pelvi-ureteric junction (PUJ) - where renal pelvis meets ureter
  2. pelvic brim
  3. vesico-ureteric junction (VUJ) - where ureter meets bladder
278
Q

classical presentation of kidney stones

A

ACUTE RENAL COLIC - severe flank (lower back) pain that radiates to the ipsilateral groin “loin to groin”
pain can come in waves

279
Q

apart from renal colic, what sx can kidney stones present with?

A
  • N&V
  • urinary frequency/urgency
  • dysuria
  • testicular pain
  • rigours
  • fever
280
Q

initial and diagnostic investigations for kidney stones

A

INITIAL
1. urine dipstick - may be haematuria
2. MSU
3. bloods - FBC, CRP & ESR, renal function (creatinine), calcium (high)

DIAGNOSTIC = NCCT KUB

281
Q

initial management for all renal/uretic stones

A

hydration, strong analgesic - IV/IM diclofenac (if contraindicated, IV paracetemol)

watchful waiting
abx if infection e.g. IV gent

282
Q

imaging of choice in kidney stones in pregnant women/children

A

ultrasound

283
Q

management of renal stones
a) <5mm and asymptomatic
b) 5-10mm
c) 10-20mm
d) >20mm

A

a) watchful waiting
b) shockwave lithotripsy
c) shockwave lithotripsy OR ureteroscopy
d) percutaneous nephrolithotomy

284
Q

management of renal stones
a) <5mm and asymptomatic
b) 5-10mm
c) 10-20mm
d) >20mm

A

a) watchful waiting
b) shockwave lithotripsy
c) shockwave lithotripsy OR ureteroscopy
d) percutaneous nephrolithotomy

285
Q

how can distal ureteric stones <10mm be managed?

A

alpha blockers e.g. tamsulosin - medical expulsion!

286
Q

what type of vulval cancer is most common?

A

squamous cell carcinoma

287
Q

what age group is vulval cancer most common in?

A

older women - >65

288
Q

RFs for vulval cancer (5)

A
  1. advanced age
  2. immunosuppression
  3. HPV infection
  4. lichen sclerosus
  5. vulvar intraepithelial neoplasia (VIN)
289
Q

what is vulvar epithelial neoplasia (VIN)?
what are the two types and what are these types associated with? in what age groups?

A

a premalignant condition

  1. high grade - type associated with HPV, women aged 35-50
  2. differentiated - alternative type, associated with lichen sclerosus, women aged 50-60

diagnosed with biopsy

290
Q

give an example of when a vulval cancer may be found incidentally

A

when catheterising an older lady with dementia

291
Q

signs and symptoms of vulval cancer

A
  1. vulval LUMP - commonly on labia majora
    - ulceration
    - bleeding
    - fungating lesion
  2. may be pain but may not
  3. itching
  4. lymphadenopathy in groin
292
Q

investigations for vulval cancer (3)

A
  1. biopsy of lesion
  2. consider sentinel node biopsy for lymph node spread
  3. imaging for staging - CT abdo and pelvis
293
Q

management options for vulval cancer

A
  • 2-week wait cancer referral
  • options depend on stage, surgical includes:
    1. wide local excision
    2. groin lymph node dissection
    3. chemo
    4. radio
294
Q

differential diagnosis for vulval cancer

A

vulvar intraepithelial neoplasia (VIN)

295
Q

what is the most common type of vaginal cancer?

A

squamous cell carcinoma (SCC)

296
Q

what type of vaginal cancer is it likely to be if the woman presenting is…
a) >60y
b) <30y

A

a) squamous cell carcinoma
b) adenocarcinoma (much rarer)

297
Q

what causes vaginal cancer?

A

HPV infection

298
Q

which HPV types are associated with vaginal cancer?

A

16 and 18 (same as cervical cancer)

299
Q

signs and symptoms of vaginal cancer (7)

A
  1. irregular bleeding
  2. blood discharge
  3. dysuria, haematuria, frequency
  4. pelvic pain
  5. may be internal lump/swelling
  6. leg swelling
  7. tenesmus (feeling like you need a poo even if you’ve just been)
300
Q

investigations for vaginal cancer (3)

A
  1. vaginal exam
  2. speculum with swabs
  3. colposcopy
301
Q

management of small stage 1 (confined within vaginal wall) vaginal cancers

A

surgical

302
Q

management of stage 2+ vaginal cancers

A

radiotherapy, chemo, chemoradiation

303
Q

what is a prolactinoma? what does it produce?

A

the most common type of PITUITARY ADENOMA

produces an excess of prolactin

304
Q

what condition is the most common cause of hyperprolactinaemia?

A

prolactinoma

305
Q

pathophysiology of prolactinomas:
a) what does it produce?
b) what does this do to the hormonal axis?
c) consequence of this

A

a) excess prolactin
b) high prolactin acts on hypothalamus, prevents the release of GnRH. without GnRH, no stimulation of LH/FSH release from the ovaries
c) results in hypogonadotropic hypogonadism and amenorrhoea

306
Q

signs and symptoms of prolactinoma

A
  1. SECONDARY AMENORRHOEA
  2. galactorrhoea
  3. infertility
  4. reduced libido
  5. osteoporosis
307
Q

key investigation for prolactinoma

A

MRI

308
Q

how are prolactinomas managed first line?

A

dopamine agonists e.g. cabergoline, bromocriptine

309
Q

how do dopamine agonists treat the sx of a prolactinoma?

A

dopamine inhibits the release of prolactin

310
Q

management of prolactinomas if medical tx is not tolerated/working

A

surgery

311
Q

main complication of prolactinomas in females

A

infertility

PHASE 3A (11 decks)

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