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3a Exam > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

What is the most common cause of ovarian cancer?

A

Epithelial ovarian tumours

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2
Q

What are the risk factors of ovarian cancer?

A
  • Increasing age
  • Lifestyle (smoking, obesity and lack of exercise)
  • Nulliparous
  • Early menarche/ late menopause
  • BRCA1& 2
  • Endometriosis
  • Infertility
  • FHx
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3
Q

Presentation of germ cell tumours in ovarian cancer?

A
  • Common in women <35
  • Rapidly enlarging abdominal mass
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4
Q

What is the clinical presentation of ovarian cancer?

A
  • Majority in 3rd/4th stage
  • IBS (ABC):
    • Abdominal pain
    • Bloating
    • Change in bowel habits: urgency
  • Urinary frequency
  • Dyspepsia
  • Fatigue
  • Weight loss
  • Painful mass
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5
Q

Who is most affected by ovarian cancer?

A

Elderly

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6
Q

What are the investigations for ovarian cancer?

A
  • CA125 tumour marker
  • Abdominal US + CT
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7
Q

What is the staging for ovarian cancer?

A

1) Ovaries

2) One/both ovaries + pelvic extension/implants

3) One/both ovaries + microscopically confirmed peritoneal implants outside pelvis

4) One/both ovaries + distant metastasis

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8
Q

What is the management of ovarian cancer?

A

Abdominal hysterectomy + bilateral salpingo-oopherectomy

Chemotherapy: stages 2-4

Radiotherapy

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9
Q

What is endometrial cancer?

A

Cancer of the endometrium (lining of the uterus)
Oestrogen dependent tumour
Includes myometrial sarcoma

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10
Q

What is the pathophysiology of endometrial cancer?

A

Unopposed oestrogen → endometrial hyperplasia → increased risk of endometrial adenocarcinoma

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11
Q

What are the risk factors for endometrial cancer?

A

Prolonged exposure of unopposed oestrogen:
- Obesity
- Diabetes
- Nulliparity
- Late menopause
- HRT
- Pelvic irradiation

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12
Q

What is the most common type of endometrial cancer?

A

Adenocarcinomas

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13
Q

What are the two types of endometrial cancer?

A

Type 1= Oestrogen dependent endometrioid carcinomas

Type 2= Oestrogen-independent non-endometrioid carcinomas

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14
Q

Who does endometrial cancer affect the most?

A

Majority >50 years old

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15
Q

What is the most common type of gynaecological cancer?

A

Endometrial cancer

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16
Q

What is the clinical presentation of endometrial cancer?

A
  • Post-menopausal bleeding/abnormal uterine bleeding
  • Menorrhagia/oligomenorrhea in pre-menopausal
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17
Q

What are the investigations for endometrial cancer?

A
  • Pelvic and abdominal examination
  • Transvaginal US: endometrial thickness >4mm
  • Endometrial pipelle biopsy: if US >4mm
  • Hysteroscopy
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18
Q

What staging is used for endometrial cancer?

A

FIGO

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19
Q

What is the management of endometrial cancer?

A
  • Total abdominal/laparoscopic hysterectomy
  • Bilateral salpingo-oopherectomy
  • Post-operative chemotherapy
  • Pelvic lymph node removal
  • Adjuvant radiotherapy + progesterone therapy
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20
Q

What are the causes of cervical cancer?

A

Human papillomavirus (HPV)

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21
Q

What is Cervical Intraepithelial Neoplasia (CIN)?
AKA cervical dysplasia

A

Abnormal cervical cell growth that can potentially lead to cervical cancer

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22
Q

Describe 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 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

Abnormal nucleus: the abnormal epithelial cell in cervical smears

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25
Q

What test would you order if you see borderline/mild dyskaryosis in a smear?

A

Test for HPV:
- -ve = back to routine screening
- +ve= colposcopy

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26
Q

What test would you order if you see moderate dyskaryosis in a smear?

A
  • Urgent colposcopy: within 2 weeks
  • Consistent with CIN II
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27
Q

What test would you order if you see severe dyskaryosis or suspected invasive cancer?

A
  • Urgent colposcopy: within 2 weeks.
  • Consistent with CIN III
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28
Q

What test would you order if you see inadequate smears?
What if they keep being inadequate?

A
  • Inadequate = repeat smear
  • Consistently inadequate = colposcopy
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29
Q

Why is the incidence of cervical cancer decreasing?

A
  1. Screening: cervical smears
  2. HPV vaccine
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30
Q

What is the most common type of cervical cancer?

A

Squamous cell

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31
Q

What are the risk factors for cervical cancer?

A
  • Persistent HPV infection
  • Early intercourse (<16yrs)
  • STI’s
  • Multiparty
  • Multiple sexual partners
  • Smoking (limits ability to clear HPV)
  • Immunosuppression
  • COCP
  • Non-attendance of cervical screening programme
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32
Q

What % of cervical cancers are found through screening?

A

30%

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33
Q

What age group does cervical cancer primarily affect?

A

25-34

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34
Q

What is the clinical presentation of cervical cancer?

A
  • Pelvic mass
  • Vaginal discomfort/urinary symptoms
  • Vaginal discharge
  • Red or white patches on cervix
  • Haematuria
  • Abnormal vaginal bleeding
  • Post-micturition bleeding
  • Post-coital bleeding
  • Polyuria
  • Haematuria
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35
Q

What is the red flag symptom for cervical cancer?

A

Post-coital bleeding

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36
Q

What are the investigations for cervical cancer?

A
  • Bimanual examination (rough and hard cervix)
  • CA125 tumour marker
  • Trans-vaginal USS
  • Calculate the RMI (risk of malignancy index): if >250 = 2 week wait referral
  • Colposcopy + cystoscopy
  • Punch biopsy
  • CT: metastasis
  • PET: for staging (FIGO)
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37
Q

What type of staging is used for cervical cancer?

A

FIGO

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38
Q

What is the management of cervical cancer?

A
  • <2cm: loop removal
  • > 2cm: radical hysterectomy
  • > 4cm: radiotherapy + chemotherapy + palliative care
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39
Q

What must you consider when treating cervical cancer?

A

Fertility

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40
Q

What is the cause of vulval cancer?

A

Vulval intraepithelial neoplasia

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41
Q

What is the most common form of vulval cancer?

A

Squamous

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42
Q

What is the clinical presentation of vulval cancers?

A
  • Vulval itch/sore
  • Persistent lump
  • Post-menopausal bleeding
  • Painful micturition
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43
Q

What is the management of vulval cancers?

A
  • Surgery: radical or conservative
  • Radiotherapy
  • Chemotherapy
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44
Q

What is the cause of vaginal cancers?

A
  • HPV
  • Metastatic spread from cervical/uterine
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45
Q

What are the symptoms of vaginal cancer?

A

Bleeding

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46
Q

What is the treatment of vaginal cancers?

A

Radiotherapy

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47
Q

What is the prognosis of vaginal cancers?

A

Poor

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48
Q

What is the pathophysiology of BRACA1/2 genes in breast cancer?

A

Faulty BRCA1 and 2 gene (tumour suppressant) increases risk of breast cancer

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49
Q

What are the majority of carcinomas split into?

A

1) Ductal OR lobular
2) In situ (not penetrating BM) OR invasive

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50
Q

What can In situ ductal carcinomas progress into?

A

Invasive

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51
Q

What is the most common breast invasive breast cancer?

A

Invasive ductal: oestrogen receptor positive

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52
Q

What staging is used in breast cancer?

A

TMN:
- Tumour
- T0= No evidence primary
- T1= <2 cm
- T2= 2-5 cm
- T3= >5 cm
- T4= Extends to chest wall or skin or inflammatory
- Nodes
- N0= No Nodes
- N1= Mobile Nodes
- N2= Fixed/matted nodes
- N3= Internal Mammary nodes
- Metastasis
- M0= No Metastases
- M1= Metastases

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53
Q

What’s the referral criteria for breast cancer?

A

2WW= >30 with breast lump ± pain

2WW= >50 with 1 of: discharge, retraction OR concerning nipple

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54
Q

What is the screening for breast cancer?

A

50-71yrs Mammogram:
- Satisfactory
- Unsatisfactory
- Unclear

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55
Q

What are the modifiable and non-modifiable risk factors for breast cancer?

A

Modifiable:
- Weight
- Exercise
- Smoking
- Alcohol
- HRT

Non-modifiable:
- Age
- Breast density
- Menopause age
- BRCA1& 2

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56
Q

Why is the incidence of breast cancer thought to be increasing?

A
  1. Western lifestyle
  2. Screening
  3. Increasing life expectancy
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57
Q

What is the clinical presentation of breast cancer?

A

May be asymptomatic in early stages
Breast and/or axillary lump: normally painless
Irregular
Hard/firm
Fixed to skin/muscle
Breast skin:
- Change to normal appearance
- Skin tethering
- Oedema
- Peau d’orange: thickened and dimpled skin
Nipples:
- Inversion
- Discharge (especially if bloody)
- Dilated veins
- Paget’s disease of the nipple
Features of metastatic spread (2Ls 2BS; bone, liver, lung, brain)

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58
Q

What is the triple assessment in breast cancer?

A

Triple assessment:
- Mammography
- High resolution US
- Core needle biopsy

Scored against:
- Clinical score: 1-5
- Imaging score: 1-5
- Biopsy score: 1-5
Followed by MDT meeting

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59
Q

What are the investigations you can order for breast cancer?

A

Triple assessment
MRI/US breast
Receptor testing:
- Oestrogen receptor status
Genetic testing (BRCA2)
FBC, CRP, ESR
Sentinel node biopsy

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60
Q

What biopsy should you do to ensure that the breast cancer hasn’t spread to the axillary lymph nodes?

A

Sentinel node biopsy

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61
Q

What is the tumour marker for breast cancer?

A

CA 15-3

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62
Q

What can microcalcifications indicate on a mammogram?

A

Ductal Carcinoma In Situ (DCIS)

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63
Q

Give 4 treatment options for patients with breast cancer

A
  1. Conservative surgery + radiotherapy
  2. Mastectomy + radiotherapy
  3. Mastectomy + reconstruction + radiotherapy (BUT can damage a lot of reconstructions)
  4. Axillary lymph node removal (limited or full)

+ Adjuvant trastuzumab, tamoxifen OR anastrozole

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64
Q

When would you perform breast conservation in breast cancer?

A
  • Small tumour relative to breast size (<25%)
  • Pre-op chemotherapy and radiotherapy also offered
  • Contradicted if under nipple
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65
Q

When would you perform a mastectomy in breast cancer?

A
  • Large tumour relative to breast size
  • Tumour underneath nipple/ in drawing nipple
  • More than one cancer in same breast
  • Delayed reconstruction
  • Patient choice
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66
Q

What percentage of breast cancers have axillary disease?

A

40%

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67
Q

When would you use full-axillary clearance in breast cancer?

A

If glands are clinically involved
No need for further surgery

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68
Q

What are the complications of full-axillary clearance in breast cancer?

A
  • Lymphedema
  • Seromas
  • Arm stiffness
  • Drain
  • Axillary numbness
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69
Q

When would you perform limited axillary surgery in breast cancer?

A

Glands are clinically normal

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70
Q

What are the benefits of limited surgery in breast cancer?

A
  • Day surgery
  • No significant complications
  • No drains
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71
Q

What medication would you offer HER-2+ve breast cancer post-op?

A

Biologic: a HER2 monoclonal antibody
- Trastuzumab

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72
Q

What medication would you offer ER/PR+ve breast cancer post-op for women:
- Pre-menopausal?
- Post-menopausal?

A

Endocrine therapy:
- Pre= Tamoxifen (inhibits oestrogen receptors on breast cancer cells)
- Post= Anastrozole (aromatase inhibitor; prevents androgens → oestrogen conversion)

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73
Q

When in breast cancer would you offer:
- Radiotherapy?
- Chemotherapy?

A

Radiotherapy: lumpectomy + aggressive after mastectomy

Chemotherapy: aggressive + high risk (e.g young age, HER-2 +ve, triple-negative receptor, Grade 3, Node +ve and tumour size)

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74
Q

Who is atrophic vaginitis common in and why?

A

Post-menopausal women due to falling levels of oestrogen

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75
Q

What are the causes of atrophic vaginitis?

A
  • Menopause
  • Oophorectomy
  • Anti-oestrogen treatments (e.g Tamoxifen and Anastrozole )
  • Radiotherapy
  • Chemotherapy
  • Post-partum: reduced oestrogen levels
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76
Q

What changes are seen to the vaginal mucosa when oestrogen falls?

A
  • Thinner
  • Drier
  • Less elastic
  • More fragile
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77
Q

When oestrogen levels fall, what changes are seen to the vaginal epithelium?

A

Inflammation →urinary symptoms

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78
Q

When oestrogen levels fall, this changes vaginal pH, flora and periurethral tissues.
Why is this bad?

A
  • Vaginal pH/flora: UTI’s or vaginal infections
  • Periurethral tissues: pelvic laxity and stress incontinence
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79
Q

What is the clinical presentation of atrophic vaginitis?

A
  • Vaginal dryness
  • Burning/itching of vagina
  • Dyspareunia
  • Vaginal discharge
  • Post-menopausal bleeding
  • Reduced pubic hair
  • Painful vaginal examination
  • Lack of vaginal folds
  • Polyuria
  • Nocturia
  • Dysuria
  • UTIs
  • Stress/urgency incontinence
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80
Q

Which investigations are used for atrophic vaginitis?

A
  • Diagnosis of exclusion
  • TVS: rules out pathology
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81
Q

What is the management of atrophic vaginitis?

A
  • Vaginal lubricants and moisturisers
  • Vaginal oestrogen
  • HRT
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82
Q

What are fibroids?

A

Benign tumours of uterine myometrium smooth muscle cells

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83
Q

What are fibroids stimulated by?

A

Oestrogen and progesterone

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84
Q

Why may fibroids go through benign degeneration and calcification?

A

Centre of larger fibroids not receiving adequate blood supply

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85
Q

How are fibroids classified?

A
  • Intramural
  • Submucosal
  • Subserosal
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86
Q

What is the most common type of fibroid?

A

Intramural

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87
Q

Define intramural fibroids

A

Growing within the endometrium

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88
Q

Define submucosal fibroids

A

Growing into the uterine cavity (can be pedunculated and may protrude through cervical os)

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89
Q

Define subserosal fibroids

A

Growing outwards from the uterus (abdominal)

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90
Q

What causes fibroids?

A
  • Acquired genetic change
  • Hormones
  • Growth factors
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91
Q

What are the risk factors for fibroids?

A
  • Obesity
  • Early menarche
  • Afro-caribbean
  • 30-40 yrs
  • FHx
  • COCP
  • Pregnancy
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92
Q

What is the most common indication for a hysterectomy?

A

Fibroids

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93
Q

What is the clinical presentation of fibroids?

A
  • Asymptomatic
  • 30-50 yrs
  • Infertility/sub-fertility
  • Menorrhagia
  • Pressure symptoms e.g. urinary frequency if pressing on bladder
  • Menorrhagia → Iron deficiency anaemia → lethargy and pallor
  • Pelvic pain
  • Recurrent miscarriages
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94
Q

What may be found on a physical examination for fibroids?

A

Palpable abdominal mass arising from pelvis

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95
Q

What investigations are ordered for fibroids?

A
  • Abdominal + bimanual examination: palpable abdominal mass arising from pelvis
  • Pregnancy test
  • FBC (anaemia)
  • TVUS
  • MRI: if US not definitive
  • Hysteroscopy
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96
Q

What is the management for fibroids?

A

Conservative: watch and wait
Suppression of ovarian function for at least 6 months:
- Mirena coil: 1st line
- COCP: e.g. triphasing (3 months continuous then break)
- Medroxyprogesterone acetate (injectable contraception)
- Progestogens: norethisterone (no bleeding)
- POP: e.g. mini pill (no bleeding)
Anti-fibrinolytics: e.g. Tranexamic acid (during bleeding)
NSAIDS: e.g. Mefanamic acid (during bleeding)
GnRH agonist: e.g. Goserelin (max 6 months)
Myomectomy
Hysterectomy (only cure for fibroids in women who have completed their family)
Ulipristal acetate (shrinks fibroid)

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97
Q

When would you do a myomectomy in fibroids?

A
  • Excessively enlarged uterine size
  • Pressure symptoms
  • Symptoms uncontrolled by medication
  • Subfertility
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98
Q

Name a GnRH agonist and its cons for use in fibroids

A

Goserelin: shrinks fibroids, but then they regrow once discontinued

Not a long term option- demineralises bone

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99
Q

What is ulipristal acetate and when is it used in fibroids?

A
  • Selective progesterone receptor modulator
  • Shrinks fibroids and induces amenorrhoea
  • Used before surgery and as an emergency contraception
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100
Q

What is the gold standard treatment for uterine fibroids?

A

Hysterectomy

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101
Q

What are the three main types of ovarian cysts?

A
  • Benign (70%)
  • Functional (24%)
  • Malignant (6%)
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102
Q

Name some benign neoplastic ovarian cysts

A
  • Benign epithelial neoplastic cysts
  • Benign neoplastic cystic tumours of germ cell origin
  • Benign neoplastic solid tumours (Fibroma <1% malignant)
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103
Q

Name some benign fibrous ovarian cysts

A
  • Adenofibroma
  • Teratoma
  • Brenner tumour
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104
Q

What are brenner tumour ovarian cysts?

A

Brenner tumours are part of the surface epithelial-stromal tumour group of ovarian neoplasms.
Majority benign

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105
Q

Name some causes hormone secreting tumours ovarian cysts

A
  • Virilisation
  • Menstrual irregularities
  • Post-menopausal bleeding
106
Q

What are 5 risk factors for ovarian cysts?

A
  • Obesity
  • Tamoxifen
  • Early menarche
  • Infertility
  • Dermoid cysts: can run in families (teratomas)
107
Q

Who does ovarian cysts primarily affect?

A

Pre-menopausal women

108
Q

What is the most common ovarian cysts type?

A

Benign neoplastic cystic tumours of germ cell origin

109
Q

What is the clinical presentation of ovarian cysts?

A
  • Chronic
  • Pain
  • Unilateral dull ache in the abdomen (intermittent or only coital pain)
  • Lower back pain
  • Dyspareuria
  • Irregular vaginal bleeding
  • Rupture/torsion = severe abdo pain + fever
  • Large cysts = abdominal swelling or pressure effects on bladder
110
Q

What are complications of ovarian cysts?

A
  • Torsion
  • Infarction
  • Hhaemorrhage
111
Q

What investigations are ordered for ovarian cysts?

A
  • Abdominal examination: swollen abdomen with palpable mass + dull to percussion
  • Pregnancy test
  • FBC: infection/haemorrhage
  • TVS/USS
  • CT/MRI: if USS not definitive
  • Diagnostic laparoscopy
  • Serum CA125 levels
112
Q

What would ascites suggest in ovarian cancer?

A

Malignancy

113
Q

For suspected ovarian cancer we do a Risk of Malignancy Index (RMI)

What does this consist of?

A

USS score + menopausal status + serum CA125 levels

114
Q

In the RMI we do a USS score.
What findings are involved in this (out of 5)?

A

USS scores 1 point for each of the following:
- Multi ocular cysts
- Solid areas
- Metastases
- Ascites
- Bilateral lesions

115
Q

How would Rokitansky’s Protuberance appear on histopathology?

A

A solid protuberance from a mature dermoid cyst (teratoma).
Contains calcific, dental, adipose, hair and/or sebaceous components.
Region has the highest propensity to undergo malignant transformation.

116
Q

What is the is management of Small, Moderate and Large Ovarian Cysts?

A

Cystectomy
Oopherectomy
Acute onset of symptoms: hospital admission
- Small (<50mm): do not require follow up
- Moderate (50-70mm): yearly US follow up
- Large: furtherMRI imaging

117
Q

What are the complications of a Ovarian Cyst rupture?

A

-Peritonitis
-Shock

118
Q

What is the clinical presentation of Ovarian Torsion?

A
  • Sudden onset deep unilateral colicky pain (brought on by exercise)
  • Iliac fossa pain radiating to loin, groin or back
  • Unilateral tender adnexal mass on examination
  • Pain may improve after 24hrs (when the ovary is dead)
  • localised tenderness
  • Palpable mass
  • Fever
  • N&V
119
Q

What investigations are ordered for Ovarian Torsion?

A
  • Ultrasound: oedema (due to venous supply cut off) + whirlpool sign (twisting/volvulus)
  • Laparoscopy
120
Q

What is the management for Ovarian Torsion?

A

Laparoscopic detorsion
Laparoscopic oophorectomy

121
Q

What is Mittelschmerz?

A

Ovulation pain (abdominal) that can last up to 48 hours

Usually unilateral pain

122
Q

What is endometriosis?

A

Chronic oestrogen-dependent condition
Endometrial tissue growth outside the uterine cavity

123
Q

Where can endometriosis occur?

A
  • Pelvic cavity (including ovaries)
  • Uterosacral ligaments
  • Pouch of Douglas
  • Recto-sigmoid colon
  • Bladder
  • Distal ureter
  • Lungs
124
Q

What is the cause of endometriosis?

A
  • Retrograde menstruation
  • Impaired immunity (retrograde tissue isn’t destroyed)
125
Q

What are the risk factors of endometriosis?

A
  • Early menarche
  • Late menopause
  • Delayed childbearing
  • Short menstrual cycles
  • Obstruction to vaginal outflow
  • Fallopian or uterus defects
  • Genetic predisposition
  • Alcohol use
  • Low body weight
126
Q

What are protective factors against endometriosis?

A
  • Multiparity
  • COCP
127
Q

Who does endometriosis affect the most?

A
  • Higher prevalence in infertile women
  • Exclusive to women of reproductive age
128
Q

Why does endometriosis improve after menopause?

A
  • Endometriosis relies on oestrogen
  • Oestrogen falls after menopause
129
Q

What is the classic triad of symptoms found in endometriosis?

A
  • Dysmenorrhoea- pain often starts days before bleeding
  • Deep dyspareuria
  • Cyclical or chronic pelvic pain

(Chronic/constant inflammation brings pain)

130
Q

What is the clinical presentation of endometriosis outside of the triad?

A
  • Sub fertility
  • Dysuria
  • Bloating
  • Lethargy
  • Constipation
  • Lower back pain
  • Dyschezia
  • Lump
131
Q

What investigations are ordered for endometriosis?

A

Gold= Laparoscopy with biopsy
- Bimanual examination: fixed, retroverted uterus
- Transvaginal US
- MRI good: if bowel involved

132
Q

What grading classification is used in endometriosis?

A

AFS

133
Q

What non-specific protein marker might be raised in a woman with endometriosis?

A

CA125

Non-specific: anything that irritates the peritoneum

134
Q

What is the management of endometriosis?

A

Suppression of ovarian function for at least 6 months:
- Mirena coil: 1st line
- COCP: e.g. triphasing (3 months continuous then break)
- Medroxyprogesterone acetate (injectable contraception)
- Progestogens: norethisterone (no bleeding)
- POP: e.g. mini pill (no bleeding)
Anti-fibrinolytics: e.g. Tranexamic acid (during bleeding)
NSAIDS: e.g. Mefanamic acid (during bleeding)
GnRH agonist: e.g. Goserelin (max 6 months)
NSAIDs/Paracetamol: for pain
Laparoscopic excision or ablation
Hysterectomy + salpingo-oophorectomy (last resort)

135
Q

How would you treat endometriosis in a woman who is wanting to get pregnant?

A

Surgery

136
Q

What is Adenomyosis?

A

The invasion of endometrial tissue into the myometrium

137
Q

Compare the epidemiology of Adenomyosis to Endometriosis.

A

Adenomyosis: older, multiparous women

Endometriosis: younger, nulliparous women

138
Q

Give 3 symptoms of adenomyosis

A
  1. Menorrhagia
  2. Dysmenorrhoea
  3. Dyspareunia (cyclical)
139
Q

What investigations might you do to confirm adenomyosis?

A
  1. Transvaginal USS
  2. MRI
  3. Hysterectomy: definitive
140
Q

What is the treatment for adenomyosis?

A

Hysterectomy

141
Q

What is polycystic Ovarian Syndrome (PCOS)

A

Polycystic ovaries + systemic symptoms causing reproductive, metabolic and psychological disturbances

142
Q

What is the pathophysiology of PCOS?

A

Excessive androgen production by theca cells of the ovaries due to either:
1) Hyperinsulinaemia
2) High luteinising hormone (LH) levels

143
Q

How does hyperinsulinaemia produce excess androgens in PCOS?

A

1) Insulin resistance → weight gain → further insulin resistance → increased androgen production
2) Reduced production of sex hormone-binding globulin (SHBG) in the liver
3) Free testosterone subsequently raised

144
Q

Why does hyperinsulinaemia cause increased androgen production PCOS?

A

1) Insulin mimics the action of insulin growth factor 1 (IGF-1) n response to LH via theca cells.
2) Insulin decreases levels of SHBG → increased free testosterone

145
Q

Why may you have raised LH?

A
  • Increase production in the anterior pituitary
  • Genetic conditions: e.g. Turner syndrome or Klinefelter syndrome
146
Q

What is the classic triad of symptoms seen in PCOS?

A

1) Oligomenorrhoea (<9 periods/year) /Amenorrhoea
2) Infertility/subfertility
3) Signs of androgen production (excess testosterone):
- Acne
- Hirsutism
- Deep voice
- Alopecia
- Male pattern balding
- Reduced breast size

147
Q

Name some signs of insulin resistance in PCOS

A
  • Acanthosis nigricans
  • Psychological symptoms (depression, mood swings, anxiety or poor self-esteem)
  • Obesity
  • Sleep apnoea
148
Q

What is the commonest cause of secondary infertility?

A

PCOS

149
Q

What is the rotterdam diagnostic criteria for PCOS?

A

2/3= PCOS
SHOP
Strings of pearls on US: Polycystic ovaries (>12 in one ovary)/ ovarian volume >10cm3
Hyperandrogenism: clinically or biochemically:
Oligomenorrhoea/ Anovulation
Prolactin normal

150
Q

What biochemical results would you expect in PCOS?

A
  • Raised testosterone
  • low SHBG
  • Raised LH levels (1:1 ratio to FSH)
  • Impaired glucose tolerance (insulin resistance)
151
Q

Which hormone is always normal when testing for PCOS?

A

Prolactin

152
Q

What is the management of PCOS?

A

TREAT THE SYMPTOMS
Encourage weight loss:
- Orlistat
- Lifestyle
Acne and hirsutism:
- COCP
- Co-cyprindol /Eflornithine
- SEVERE= Isotretinoin
For pregnancy (need 4 periods a year to develop lining of the womb):
- Clomifene (anti-oestrogen)/tamoxifen.
- Metformin: increases insulin sensitivity
- Letrozole
- Laparoscopic ovarian drilling or gonodotrophins

153
Q

What is Menopause?

A

Permanent cessation of menstruation due to loss of follicular activity for 12 months

154
Q

Define peri-menopause.

A

The period leading up to the menopause: irregular periods and symptoms

155
Q

What is the average age of menopause?

A

40-60 (average 51)

156
Q

If a woman goes through menopause <50, for how many years is she still fertile for?

A

2 years

157
Q

If a woman goes through menopause >50, for how many years is she still fertile for?

A

1 year

158
Q

What is the pathophysiology of menopause?

A

Reduction in oocytes → decreased ovarian production of progesterone, estradiol, testosterone and fertility

159
Q

A depletion in what hormone is thought to trigger the symptoms of the menopause?

A

Oestrogen

160
Q

What are the consequences of menopause?

A
  • CV disease (cause of death of 1/3 of women)
  • Vasomotor symptoms
  • Urogenital problems: due to oestrogen deficiency
  • Osteoporosis
161
Q

What are the early signs of menopause?

A
  • Oligomenorrhea
  • Vasomotor:
  • Hot flushes
  • Night sweats
  • Palpitations
  • Vaginal dryness
  • Reduced libido
  • Poor concentration and fatigue
  • Headaches
  • Joint pain
162
Q

What are 3 ongoing signs of menopause?

A
  • GU symptoms (frequency, urgency, dyspareunia, incontinence and UTIs)
  • Atrophic vaginitis
  • PMB
163
Q

What are the 3 late signs of menopause?

A
  • Osteoporosis
  • CVD
  • Dementia
164
Q

What investigations are ordered in menopause?

A

Bloods:
- Raised FSH = fewer oocytes
- Anti-mullerian hormone = ovarian reserve
DEXA scan: bone density estimation

165
Q

What is the management of menopause?

A
  • Lifestyle advice
  • Reduce modifiable RF’s
  • HRT
  • Bisphosphonates: osteoporosis
  • Vaginal oestrogens
  • Progesterone, Clonidine, SSRIs: hot flushes and night sweats
  • Non-hormonal options e.g. clonidine
  • Non-pharmaceutical e.g. CBT
166
Q

What are the pros and cons of HRT?

A

Pros:
- Symptom management
- Osteoporosis prevention
- Colo-rectal cancer prevention

Cons:
- Risk breast Ca: if COCP
- Risk of endometrial Ca- if oestrogen only
- Risk of gallbladder disease
- Risk of VTE
- Risk of CV disease

167
Q

What is a ectopic pregnancy?

A

Pregnancy implanted outside the uterus

168
Q

What is the clinical presentation of a ectopic pregnancy?

A

Acute
6-8 weeks of Amenorrhoea
Lower abdominal pain
Shoulder tip pain
Late vaginal bleeding
Cervical excitation

169
Q

What are common symptoms of a:

Appendicitis?

A

Acute
Colicky abdominal pain and guarding:
- Central abdomen pain that localises to the RLF within 24 hours
- Due to visceral →parietal peritoneum irritation
Low grade pyrexia
Tachycardia + Dyspnoea= perforation
N&V: anorexia
Foetor oris
Constipation/diarrhoea
Rebound and percussion tenderness at McBurney’s point: peritonitis
Appendix mass may be palpable in RIF
Pain PR suggests pelvic appendix
Rovsing’s sign
Psoas sign
Cope sign

170
Q

What is Pelvic Inflammatory Disease?

A

Infection and inflammation of the female pelvic organs

171
Q

What usually causes PID?

A

Ascending infection from the cervix e.g.
- Chlamydia
- Gonorrhoea
- +/- E.coli

WORRIED ABOUT GROUP A STREP

172
Q

What are the risk factors for Pelvic Inflammatory Disease?

A
  • Young
  • New sexual partner
  • Lack of barrier contraception
  • Lower socio-economic group
  • TOP
  • IUD
173
Q

What is the clinical presentation of Pelvic Inflammatory Disease?

A
  • Bilateral lower abdominal pain
  • Acute
  • Pelvic pain
  • Fever
  • Deep dyspareunia
  • Purulent discharge
  • Dysuria
  • Amenorrhea
  • Oligomenorrhea
  • Cervical excitation on examination
174
Q

What are the investigations of Pelvic Inflammatory Disease?

A
  • Pregnancy test
  • Cervical swabs
  • Elevated ESR & CRP
  • Endometrial biopsy
  • USS
  • Urinalysis
  • Laparoscopy: direct visualisation of fallopian tubes
175
Q

What is the treatment for PID?

A
  • Ceftriaxone (1 dose IM) + doxycycline (2 doses PO) + metronidazole (BD for 14 days PO)
  • Remove IUD
176
Q

Define menstruation

A

Monthly bleeding from the reproductive tract due to hormonal changes

177
Q

Define Menarche?

A

Last manifestation of puberty following development of secondary sex characteristics by oestrogen

178
Q

What causes a menstrual cycle?

A

Hormonal changes causes ovulation and induce endometrial change to prepare for implantation

179
Q

Describe the hypothalamic- pituitary axis

A

Hypothalamus → GnRH → FSH + LH → Ovaries release oestrogen + progesterone

Oestrogen + progesterone → negative feedback on hypothalamus + anterior pituitary

180
Q

What happens in days 1-4 of the menstrual cycle?

A
  • Hormonal support withdrawn
  • Endometrium sheds
  • Sometimes painful myometrial contraction
  • Raised Oestradiol causes endometrium reform and thickening
  • Positive feedback on LH = ovulation 36 hours later
181
Q

What happens on days 5-13 of the menstrual cycle?

A
  • GnRH stimulates FSH & LH
  • LH induces follicular growth → oestradiol and
    inhibin production→ FSH suppression due to negative feedback
  • Only one oocyte matures
182
Q

What happens in days 14-28 of the menstrual cycle?

A
  • Follicle becomes Corpus Luteum
  • Produces more progesterone than oestradiol → increased blood supply and endometrium enlargement
183
Q

What happens if the corpus luteum is not fertilised?

A

Corpus luteum will collapse → fall in oestrogen and progesterone

184
Q

What hormone is responsible for ‘growing’ the endometrium and what hormone ‘shrinks’ the endometrium?

A
  • Oestrogen grows
  • Progesterone shrinks
185
Q

What is premenstrual syndrome?

A

The emotional and physical symptoms women experience prior to menstruation (luteal phase)

186
Q

What is the clinical presentation of premenstrual syndrome?

A
  • Anxiety
  • Stress
  • Fatigue
  • Mood swings
187
Q

What is the management of premenstrual syndrome?

A
  • Healthy diet
  • Exercise
  • Stress reduction methods
  • Regular sleep
  • Paracetamol
  • COCP
  • SSRIs
188
Q

Define menorrhagia

A
  • Excessive menstrual blood loss (>80mL) within a normal menstrual cycle.
  • Interferes with their physical, emotional and social QOL.
189
Q

What are the causes of menorrhagia?

A
  • Most = no histological problem
  • Fibroids/polyps (majority)
  • Coagulation problems
  • Endometriosis/adenomyosis
  • Hypothyroidism
  • Infection
  • Ovulatory problems
  • Endometrial dysfunction
190
Q

What investigations are ordered for menorrhagia?

A
  • FBC
  • TSH/T4
  • Coagulation function
  • STI screen
  • B12/Folate/Iron
  • Smear if due
  • TVS: assess endometrial thickness and masses
  • Endometrial biopsy + hysteroscopy: if TVS shows endometrial thickness >10mm and >40yrs (to exclude cancer)
191
Q

What is the management of menorrhagia?

A

Conservative: watch and wait
Suppression of ovarian function for at least 6 months:
- Mirena coil: 1st line
- COCP: e.g. triphasing (3 months continuous then break)
- Medroxyprogesterone acetate (injectable contraception)
- Progestogens: norethisterone (no bleeding)
- POP: e.g. mini pill (no bleeding)
Anti-fibrinolytics: e.g. Tranexamic acid (during bleeding)
NSAIDS: e.g. Mefanamic acid (during bleeding)
GnRH agonist: e.g. Goserelin (max 6 months)
Myomectomy
Hysterectomy (only cure for fibroids in women who have completed their family)
Endometrial ablation
Resection of fibroids
Uterine artery embolization
Ulipristal acetate (shrinks fibroid)

192
Q

What is Post-Coital bleeding?

A

Non-menstrual bleeding that occurs immediately after sexual intercourse

193
Q

What are causes of Post-Coital bleeding?

A

Infection
Cervical ectropion
Polyps
Carcinoma

194
Q

What are investigations of Post-Coital bleeding?

A
  • Bimanual and abdominal examination
  • Smear
195
Q

What is primary amenorrhoea?

A
  • No menstruation by age 16.
  • Absence of secondary sexual characteristics by 14 + no menarche
196
Q

What is secondary amenorrhoea?

A

When previously normal menstruation stops for >6 months

197
Q

What are the causes of primary amenorrhoea?

A
  • Turner’s Syndrome
  • Androgen Insensitivity Syndrome
  • Congenital malformations of genital tract
  • Congenital adrenal hyperplasia
  • Imperforate hymen
198
Q

What is Oligomenorrhoea?

A

Menses >35 days apart

199
Q

Why may a low birth weight cause secondary amenorrhoea?

A
  • Low birth weight is linked to increased Ghrelin
  • Ghrelin normally inhibits the hypothalamic-pituitary ovarian axis
  • Decreased GnRH → decreased pituitary release of FSH and LH
200
Q

What are the causes of secondary amenorrhoea?

A
  • Drug induced
  • Pregnancy (breast-feed)
  • Hyperprolactinaemia (inhibits GnRH secretion)
  • Hypothyroidism
  • Ovarian causes (PCOS)
  • Pituitary tumour
  • Hypothalamic hypogonadism
201
Q

What are the investigations for secondary amenorrhoea?

A
  • BhCG (check for pregnancy)
  • FSH/LH: low
  • Prolactin
  • TFTs
  • Testosterone levels
202
Q

What would a low FSH/LH mean in amenorrhoea?

A

Hypothalamic pituitary ovarian axis pathology

203
Q

What would a high FSH/LH but low oestrogen mean in amenorrhoea?

A

Premature ovarian failure

204
Q

What is premature ovarian failure?

A

Primary ovarian insufficiency in <40yrs + menopausal symptoms

205
Q

What is the diagnostic criteria for premature ovarian failure?

A
  1. FSH >25IU/I (2 samples 4 weeks apart)
  2. 4 months of amenorrhoea
206
Q

What is the management of premature ovarian failure?

A

Cannot be reversed with HRT
- HRT/COCP: symptomatic relief + prevents osteoporosis
- Donor eggs: fertility

207
Q

What is the management of amenorrhoea due to HPO axis malformation?

A

Mild = stress/exercise (activity to stimulate enough oestrogen to produce an endometrium)
Severe = GnRH analogues

208
Q

How would you manage fertility issues caused by amenorrhoea?

A

Clomifene

209
Q

What is the pathophysiology of dysmenorrhoea?

A
  • High prostaglandin levels in the endometrium
  • Contractions
  • Uterine Ischaemia
210
Q

What are some causes of Secondary Dysmenorrhoea?

A
  • Fibroids
  • Adenomyosis
  • Endometriosis
  • PID
  • Tumours
211
Q

Name 4 reproductive disorders that are associated with obesity

A
  1. PCOS.
  2. Miscarriage.
  3. Infertility.
  4. Obstetric complications
212
Q

What is Genitourinary Prolapse?

A

Descent of 1≥ of the pelvic organs:
- Uterus/vaginal walls
- Bladder
- Rectum
- Small/large bowel
- Vaginal vault

213
Q

What is the clinical presentation of Genitourinary Prolapse?

A

Urinary
Bowel
Sexual
Local pelvic symptoms

214
Q

What are the risk factors for Genitourinary Prolapse?

A
  • Increasing age
  • Vaginal delivery
  • Increasing parity
  • High BMI
  • Spina bifida and spina bifida occulta
  • Pelvic mass
  • Menopause
  • Iatrogenic (pelvic surgery)
215
Q

What is the pathophysiology of Genitourinary Prolapse?

A
  • Pelvic organs losing their structure through muscle trauma, neuropathic injury or stretching.
  • Orientation and shape of pelvic bones
216
Q

Name the three anterior compartment prolapses

A

1) Urethrocele (urethra → vagina)

2) Cystocele (bladder → vagina)

3) Cystourethrocele (both)

217
Q

Name the three middle compartment prolapses

A

1) Uterine prolapse (→ vagina)
2) Vaginal vault prolapse (descent of vaginal vault post hysterectomy)
3) Enterocele

218
Q

What is an enterocele?

A

Pouch of Douglas (small bowel) into the vagina

219
Q

What is a posterior compartment prolapse?

A

Rectocele (rectum into the vagina)

220
Q

What are the 4 stages of vaginal prolapse?

A

Stage 1: >1cm above the hymen

Stage 2: within 1cm proximal/distal of the hymen

Stage 3: >1cm below the plane of the hymen, but protrudes no further than <2cm of the total length of the vagina

Stage 4 : complete eversion of the vagina

221
Q

What is the clinical presentation of Genitourinary Prolapse?

A
  • Older women
  • Asymptomatic
  • Dragging down, pressure and heaviness
  • Pain
  • Lump
  • Discomfort
  • Dyspareuria
  • Urinary symptoms: incontinence, frequency and urgency (anterior symptoms)
  • Constipation/straining (posterior symptoms)
222
Q

What investigations are ordered for Genitourinary Prolapse?

A
  • Assessment of post-void residual urine (PVR) volume
  • Assessing pelvic floor muscles- bimanual examination + exclude pelvic masses
  • Urinalysis
  • Urodynamics
  • Bladder diaries
  • Symptom scoring and quality-of-life assessment
  • Measure post-void residual volume by bladder scan or catheterisation
  • Defecography, anal manometry and endoanal ultrasound (constipation or faecal incontinence)
  • Imaging + cystoscopy as a last resort
223
Q

What is the management of Genitourinary Prolapse?

A

CONSERVATIVE (reduction of intrabdominal pressure):
- Weight loss
- Stop smoking
- Reduce straining i.e constipation or heavy lifting
- Pelvic floor muscle exercises
- Vaginal pessaries e.g. ring
Surgical (last resort):
- Hysterectomy
- Colporrhapy (all prolapse tx)
- Colposuspension (stress incontinence tx)
- Sacrohysteropexy (uterine prolapse tx)
- Sacrospinous fixation (uterine prolapse tx)

224
Q

What is a sacrospinous fixation?

A
  • Stitches the top of the vagina/cervix to a pelvic ligament (sacrospinous ligament)
  • Treats uterine prolapses
225
Q

What is a sacrohysteropexy

A
  • Re-suspends the prolapsed uterus to the anterior longitudinal presacral ligament via polypropylene mesh
  • Treats uterine prolapses
226
Q

What is colposuspension?

A
  • Stitches pull up the vagina around the bladder opening
  • Treats stress incontinence
227
Q

What is a Colporrhaphy?

A
  • Repairs defective vaginal walls
  • Treats most prolapses
228
Q

Describe the epithelium of the detrusor muscle

A

Smooth muscle with transitional epithelium

229
Q

What is the nerval innervation of the detrusor muscle?

A

Parasympathetic S2-S4

230
Q

What is the functional bladder capacity?

A

400ml

231
Q

Define incontinence

A

The involuntary leakage of urine

232
Q

What are the two types of incontinence?

A

1) Urgency
2) Stress

233
Q

What is urge incontinence?

A

Overactive bladder: involuntary detrusor muscle bladder contractions

234
Q

What is stress incontinence?

A

-Weak urethral sphincter: detrusor pressure > closing pressure of urethra).
-Increase in intra-abdominal pressure results in the leakage of urine.

235
Q

What is the clinical presentation of a Overactive Bladder (urge incontinence)?

A
  • ‘Key in door’ urgency
  • Frequency
  • Nocturia
  • Enuresis
236
Q

What is the clinical presentation of Stress Incontinence?

A

Leakage on:
- Coughing
- Laughing
- Lifting
- Exercise
- Movement

237
Q

What are the causes of Stress Incontinence?

A
  • Menopause = low oestrogen = weakening pelvic support
  • Radiotherapy
  • Congenital weakness
  • Pelvic surgery
238
Q

What investigations are ordered in Incontinence?

A
  • Bimanual examination
  • MSU
  • Bladder diary (frequency volume chart).
  • Urinalysis
  • Post-void residual bladder volume e.g. catheter or USS
  • Urodynamic testing
  • ePAQ.
239
Q

What information from a urinalysis will aid you in diagnosing incontinence?

A
  • Nitrates & Leukocytes = infection
  • Haematuria= Glomerulonephritis
  • Proteinuria = Renal Disease
  • Glycouria = diabetes
240
Q

What information can you obtain from a bladder diary?

A
  1. Frequency
  2. Quantity of urine
  3. Fluid intake
  4. Diurnal variation
241
Q

How do you measure the Post-void residual bladder volume in incontinence?

A

Urine in and out of the catheter/US

242
Q

What is the ePAQ questionnaire in incontinence?

A

Explores impact on life to determine management plan

243
Q

What questions are involved in the ePAQ questionnaire in incontinence?

A

Urinary: pain, voiding, stress and overactive bladder

Vaginal: pain, capacity and prolapse

Bowel: IBS, constipation and continence

Sexual: dyspareunia and overall sex life

244
Q

What is the general management of incontinence?

A
  • Weight loss
  • Reduce caffeine
  • Smoking cessation
  • Avoid straining
  • Pads and pants
  • Catheters
245
Q

What is the management of Stress incontinence?

A

Pelvic floor exercises
Duloxetine (SNRI- antidepressant)
Surgery (supports + restores pressure to the urethra):
- Colposuspension
- Sling
- TVT (tension free vaginal tape)

246
Q

How do pelvic floor exercises work in treating someone with stress incontinence?

A
  • Pelvic floor muscle contraction → urethra compression → increased urethral pressure → reduced leakage
  • Vaginal cones can also be used
247
Q

What is the management of overactive bladder incontinence?

A

Antimuscarinics/Anticholinergics: Oxybutynin
Adrenergic agonist: Mirabegron
Botox: Botulinum Toxin
Surgery:
- Bladder Drill
- Bypass

248
Q

How does botulinum toxin work in treating OAB incontinence?

A

Blocks ACh release → reduced destrusor muscle contraction

249
Q

Give 5 side effects of oxybutynin

A
  1. Dry mouth
  2. Constipation
  3. Blurred vision
  4. Cognitive impairment
  5. Tachycardia
250
Q

Name an adrenergic agonist used in OAB

A

Mirabegron

251
Q

How does mirabegron work in treating OAB?

A
  • Beta 3 agonist
  • Relaxes the detrusor muscle and increases bladder capacity
252
Q

Where are FSH and LH produced

A

Anterior pituitary gland

253
Q

Where is GnRH produced?

A

Hypothalamus

254
Q

When LH and FSH have binding to the various cells, what is produced?

A

1) Theca cells produce Androstenedione
2) Granulosa cells produce aromatase
3) Aromatase converts Androstenedione into oestrogen
4) Oestrogen creates negative feedback to stop producing FSH
5) Once oestrogen becomes really high → becomes positive feedback to produce FSH and LH
6) Influx of FSH and LH = release of oocyte

255
Q

What effect does high oestrogen levels have on the endometrium?

A

1) Thickening of endometrium
2) Growth of endometrial glands
3) Emergence of spiral arteries to supply the released oocyte
4) Makes cervical mucus more hospitable for incoming sperm

256
Q

What is the dominant hormone in the luteal phase?

A
  • Progesterone
  • Luteinised granulosa and theca cells produce progesterone and inhibin → negative feedback on FSH/LH and oestrogen
257
Q

What does the corpus luteum become?

A

1) Corpus albicans (doesn’t produce hormones)
2) Low progesterone → spiral arteries collapse and functional layer sloughs off

258
Q

What are the two phases of the uterus in the menstrual cycle?

A
  • Days 1-14 = Menstrual/ follicular/ proliferative phase
  • Days 15-28 = luteal/ secretory phase
259
Q

Define FGM

A

Procedures involving damaging or removing external female genitalia for non-medical reasons.

260
Q

What problems can FGM cause?

A
  • Conception
  • Labour
  • Infections
  • PTSD
  • Chronic pain
  • PPH
  • Increased need for C-section and episiotomy

3a Exam (9 decks)

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