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MY REVISION - ALL PHASES > WOMENS HEALTH - GYNAE > Flashcards

WOMENS HEALTH - GYNAE Flashcards

1
Q

CONGENITAL STRUCTURES
What are congenital structural abnormalities and what are the causes?
What can it lead to?

A
  • Abnormal development of pelvic organs prior to birth, may be result of faulty genes or occur randomly in otherwise healthy people
  • Menstrual, sexual + reproductive problems
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2
Q

CONGENITAL STRUCTURES
What is the basic embryology of the female genital tract?

A
  • Upper third of vagina, cervix, uterus + fallopian tubes develop from paramesonpehric (Mullerian) ducts
  • Errors in their development can lead to congenital structural abnormalities
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3
Q

CONGENITAL STRUCTURES
Give 3 examples of congenital structural abnormalities

A
  • Bicornuate uterus
  • Transverse vaginal septae
  • Vaginal hypoplasia + agenesis
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4
Q

CONGENITAL STRUCTURES
What is bicornuate uterus?
Associations?

A
  • 2 horns to uterus giving heart-shape on pelvic USS
  • May be associated with adverse pregnancy outcomes (miscarriage, premature birth, malpresentation)
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5
Q

CONGENITAL STRUCTURES
What is a transverse vaginal septum?

A
  • Septum (wall) forms transversely across the vagina, can be perforate (with a hole) or imperforate (completely sealed)
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6
Q

CONGENITAL STRUCTURES
How does transverse vaginal septae present?

A
  • Perforate = still menstruate but difficulty with intercourse + tampon use
  • Imperforate = cyclical pelvic Sx but no menses as sealed, can lead to endometriosis by retrograde menstruation
  • May have infertility + pregnancy related issues
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7
Q

CONGENITAL STRUCTURES
What is the management of transverse vaginal septae?

A
  • Dx by examination, USS or MRI with surgical correction
  • Main complications of surgery are vaginal stenosis or recurrence
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8
Q

CONGENITAL STRUCTURES
What is vaginal hypoplasia and agenesis
What causes it?

A
  • Hypoplasia = abnormally small vagina
  • Agenesis = absent
  • Failure of Mullerian ducts to develop properly + may be associated with absent uterus + cervix
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9
Q

CONGENITAL STRUCTURES
In vaginal hypoplasia and agenesis what structure is not affected?
What is the management?

A
  • Ovaries – leading to normal female sex hormones
  • Prolonged period with vaginal dilatation for adequate size or surgery
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10
Q

MENORRHAGIA
What is menorrhagia?

A
  • Heavy menstrual bleeding that occurs at expected intervals of the menstrual cycle + interferes with QOL (no measurable quantity)
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11
Q

MENORRHAGIA
What are some causes of menorrhagia?

A
  • Unknown = dysfunctional uterine bleeding
  • Fibroids (most common cause in gynae)
  • Bleeding disorder (vWD)
  • Hypothyroidism
  • Polyps, endometriosis, adenomyosis, PID, contraceptives (IUD)
  • Endometrial hyperplasia or cancer
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12
Q

MENORRHAGIA
What are some investigations for menorrhagia?

A
  • Bimanual exam (?fibroids if bulky non-tender, ?adenomyosis if bulky tender ‘boggy’)
  • FBC for ALL women, ferritin (anaemic), TFTs, clotting screen
  • STI screen
  • Pelvic (TV>TA) USS
  • Hysteroscopy ± endometrial biopsy if ?endometrial pathology
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13
Q

FIBROIDS
What are fibroids?

A
  • Benign tumours of the smooth muscle of the uterus (uterine leiomyomas)
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14
Q

FIBROIDS
What are the different types of fibroids?

A
  • Intramural (most common) = within the myometrium
  • Subserosal = >50% fibroid mass extends outside uterine contours
  • Submucosal = >50% projection into the endometrial cavity
  • Subserosal + submucosal can be pedunculated (on stalk = risk of torsion)
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15
Q

FIBROIDS
What are the issues with intramural fibroids?

A

As they grow, they change the shape + distort the uterus

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16
Q

FIBROIDS
What can cause fibroids?

A
  • Oestrogen dependent so grow in response to it (rare before puberty or after menopause)
  • Associated with mutation in gene for fumarate hydratase
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17
Q

FIBROIDS
What are some risk factors for fibroids?

A
  • Afro-Caribbean
  • Obesity
  • Early menarche
  • FHx
  • Increasing age (until menopause)
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18
Q

FIBROIDS
What is the clinical presentation of fibroids?

A
  • Menorrhagia (#1)
  • Prolonged menstruation, deep dyspareunia
  • Lower abdo cramping pain (worse during menstruation)
  • Bloating
  • Urinary or bowel Sx due to pelvic pressure or fullness
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19
Q

FIBROIDS
What are some investigations for fibroids?

A
  • Abdo + bimanual exam = palpable pelvic mass or bulky non-tender uterus
  • FBC for ALL women (?Fe anaemia)
  • Pelvic (TV>TA) USS for larger fibroids
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20
Q

FIBROIDS
What are some complications of fibroids?

A
  • Red degeneration
  • Benign calcification if centre of larger fibroids not receiving adequate blood supply
  • Reduced fertility (submucosal interfere with implantation)
  • Obstetric issues (miscarriage, premature labour)
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21
Q

FIBROIDS
What is red degeneration of fibroids?

A
  • Ischaemia, infarction + necrosis of fibroid due to disrupted blood supply
  • Fibroids sensitive to oestrogen so can grow rapidly in presence (like pregnancy) + outgrow their blood supply > ischaemia
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22
Q

FIBROIDS
How does red degeneration of fibroids present and what is the management?

A
  • Low-grade fever, pain + vomiting (classically in pregnant woman)
  • Supportive management like analgesia, fluids
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23
Q

FIBROIDS
How is the management of fibroids split?

A
  • Fibroids <3cm
  • Fibroids >3cm (with referral to gynae for investigation + management)
  • Also split into non-hormonal + hormonal depending on if woman wants to get pregnant
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24
Q

FIBROIDS
What is the first line non-hormonal management of fibroids <3cm?

A
  • Tranexamic acid (antifibrinolytic) taken during bleeding to reduce it
  • Mefenamic acid (NSAID) to reduce bleeding + pain
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25
Q

FIBROIDS
What is the first line hormonal management of fibroids <3cm?

A
  • Mirena coil is 1st line (fibroids <3cm with no uterus distortion)
  • 2nd = COCP triphasing (back-to-back for 3m then break)
  • Cyclical oral progestogens
  • Norethisterone 5mg TDS can be used short-term to rapidly stop menorrhagia from 3d before period until bleeding acceptable
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26
Q

FIBROIDS
What is the management of fibroids <3cm that fail medical treatment or are severe?

A
  • Surgery
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27
Q

FIBROIDS
What is the management of fibroids >3cm?

A
  • Same medical Mx but surgery offered too
  • GnRH agonists (goserelin) can be given to shrink fibroids by inducing menopausal state (reduced oestrogen) in short-term (can demineralise bone) for surgery
  • Selective progesterone receptor modulators (SPRMS) like ulipristal acetate can be used instead to avoid SEs
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28
Q

FIBROIDS
What are the 5 main surgical options of managing fibroids?

A
  • Trans-cervical resection of fibroid via hysteroscopy
  • 2nd gen endometrial ablation
  • Uterine artery embolisation
  • Myomectomy
  • Hysterectomy
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29
Q

FIBROIDS
What is…

i) trans-cervical resection of fibroid?
ii) endometrial ablation?
iii) uterine artery embolisation?
iv) myomectomy?
v) hysterectomy?

A

i) Removal of submucosal fibroid, offered to women planning on having more children
ii) Destroys endometrium via radiofrequency ablation, non-hysteroscopic, day case
iii) Blocked arterial supply to fibroid starves of oxygen + shrinks
iv) Removal of fibroid via laparoscopy/laparotomy
v) Removal of uterus + fibroids ± oophorectomy depending on situation (last resort)

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30
Q

FIBROIDS
What management of fibroids is the only one considered to improve subfertility?
What is a risk of this management?

A
  • Myomectomy
  • Avoid during pregnancy or c-section as massive haemorrhage risk
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31
Q

ADENOMYOSIS
What is adenomyosis?

A
  • Endometrial tissue inside the myometrium – oestrogen dependent
  • Can occur alone or alongside endometriosis or fibroids
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32
Q

ADENOMYOSIS
What is the epidemiology of adenomyosis?

A
  • More common in later reproductive years + those who are multiparous (contrast to fibroids)
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33
Q

ADENOMYOSIS
How does adenomyosis present?

A
  • Dysmenorrhoea, menorrhagia + dyspareunia are classic Sx
  • Cyclical pain worse as period starts but can last 2w after it stops (much longer than endometriosis)
  • May cause infertility or pregnancy-related issues
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34
Q

ADENOMYOSIS
What are the investigations for adenomyosis?

A
  • Bimanual exam = bulky + tender uterus, ‘BOGGY’
  • TVS is 1st line investigation
  • Gold standard - histological examination of uterus after hysterectomy (not always suitable though)
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35
Q

ADENOMYOSIS
What are some complications of adenomyosis?

A
  • Infertility
  • Miscarriage
  • Preterm birth
  • SGA
  • PPROM
  • Malpresentation
  • PPH
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36
Q

ADENOMYOSIS
What is the initial management of adenomyosis?

A
  • Same as fibroids or menorrhagia in general
  • TXA or mefenamic acid
  • Mirena coil 1st line if no uterus distortion
  • COCP triphasing
  • Cyclical progesterone
  • Norethisterone 5mg TDS short-term
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37
Q

ADENOMYOSIS
What is the other management of adenomyosis?

A
  • GnRH analogues like goserelin to induce menopause-like state
  • Endometrial ablation, UAE or hysterectomy (if family completed)
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38
Q

ENDOMETRIOSIS
What is endometriosis?

A
  • Presence of ectopic endometrial tissue outside the uterus
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39
Q

ENDOMETRIOSIS
Where might endometriosis occur?

A
  • Pouch of Douglas > PR bleeding
  • Uterosacral ligaments
  • Bladder + distal ureter > haematuria
  • Pelvic cavity incl. ovaries > endometrioma in ovaries
  • Less common - lungs, nose, umbilicus, previous scars (lump gets big + painful)
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40
Q

ENDOMETRIOSIS
What is the pathophysiology of endometriosis?

A
  • Cells of endometrial tissue outside uterus respond to hormones in same way > oestrogen dependent condition
  • During menstruation, endometrial tissue sheds lining + bleeds leading to irritation + inflammation of nearby tissues
  • Chronic + constant inflammation > cyclical pain
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41
Q

ENDOMETRIOSIS
What is the epidemiology of endometriosis?

A
  • Higher prevalence in infertile women
  • Exclusive to women of reproductive age
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42
Q

ENDOMETRIOSIS
What are 3 theories about the cause of endometriosis?

A
  • Sampson’s = retrograde menstruation (endometrial lining flows backwards through fallopian tubes + into pelvis/peritoneum where endometrial tissue seeds itself
  • Meyer’s = metaplasia of mesothelial cells
  • Halban’s = via blood or lymphatics
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43
Q

ENDOMETRIOSIS
What are some risk factors for endometriosis?

A
  • Early menarche,
  • late menopause,
  • obstruction to vaginal outflow (imperforate hymen)
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44
Q

ENDOMETRIOSIS
What is the clinical presentation of endometriosis?

A
  • Dysmenorrhoea, deep dyspareunia + cyclical chronic pelvic pain
  • Pain worse 2–3d before periods + better after
  • Cyclical bowel + bladder Sx = pain on defecation (dyschezia), dysuria, urgency
  • Sub-fertility + cyclical bleeding from various sites
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45
Q

ENDOMETRIOSIS
What are the investigation of endometriosis?

A
  • Bimanual = ?adnexal masses or tenderness, nodules in uterosacral ligaments or fixed + retroverted uterus due to adhesions
  • TVS for ovarian endometrioma (chocolate cyst) = brown fluid as old blood + tissue
  • Gold standard = laparoscopy with biopsy
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46
Q

ENDOMETRIOSIS
What might laparoscopy and biopsy show?
What is the benefit of this investigation?

A
  • White scars or brown spots = ‘powder burn’
  • Added benefit of being able to remove deposits during procedure
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47
Q

ENDOMETRIOSIS
What are some complications of endometriosis?

A
  • Subfertility
  • Adhesions
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48
Q

ENDOMETRIOSIS
How does endometriosis cause subfertility?

A
  • Areas of endometriosis release cytokines + harmful chemicals which can damage reproductive tract
  • Can cause reduced fallopian tube motility, scarring, bleeding, toxicity to oocyte
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49
Q

ENDOMETRIOSIS
How does endometriosis cause adhesions?

A
  • Localised bleeding + inflammation causes damage + development of scar tissue that binds the organs together (adhesions)
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50
Q

ENDOMETRIOSIS
What is the initial management of endometriosis?

A
  • NSAIDs ± paracetamol first line for Sx relief
  • COCP triphasing (can’t take for longer as if not irregular bleeding
  • POP like medroxyprogesterone acetate
  • GnRH analogues to “induce” menopause, reversible, quicker than triphasing but need HRT + only short-term as risk of osteoporosis
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51
Q

ENDOMETRIOSIS
What fertility-sparing treatments are there for endometriosis?

A
  • Laparoscopic removal of adhesions either by ablation (burning) or excision (cutting) away endometriotic tissue
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52
Q

ENDOMETRIOSIS
What is the last resort treatment of endometriosis?

A
  • Hysterectomy ± bilateral salpingo-oopherectomy as no ovaries = no cycle
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53
Q

PCOS
What is polycystic ovarian syndrome (PCOS)?

A
  • Syndrome of excess androgen production by theca cells of ovaries due to hyperinsulinaemia + increased LH levels (due to pituitary production increase, genetics like Turner’s or Klinefelter’s)
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54
Q

PCOS
How does insulin resistance contribute to PCOS?

A
  • Insulin resistance = pancreas produces more insulin
  • Insulin mimics action of insulin-like growth factor 1 which augments androgen production by theca cells in response to LH
  • Higher insulin = higher androgens (testosterone)
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55
Q

PCOS
How does high insulin levels contribute to PCOS?

A
  • Insulin suppresses sex hormone-binding globulin (SHBG) produced by liver which normally binds to androgens + suppresses their function further promoting hyperandrogenism
  • Also contribute to halting development of follicles in ovaries > anovulation + multiple partially developed follicles (polycystic ovaries)
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56
Q

PCOS
What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism
  • Insulin resistance
  • Oligo or amenorrhoea + sub/infertility
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57
Q

PCOS
How does hyperandrogenism present in PCOS?

A
  • Acne, hirsutism, deep voice, male-pattern hair loss
  • Hirsutism is growth of thick, dark hair often in male pattern (facial hair)
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58
Q

PCOS
What are some differentials of hirustism?

A
  • Ovarian or adrenal tumours that secrete androgens
  • Cushing’s syndrome
  • CAH
  • Iatrogenic (steroids, phenytoin)
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59
Q

PCOS
How does insulin resistance present?

A
  • Obesity, acanthosis nigricans (thickened, rough skin often axilla + elbows with velvety texture), psychological Sx
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60
Q

PCOS
What diagnostic criteria is used in PCOS?

A

Rotterdam criteria (≥2) –
- Oligo- or anovulation (may present as oligo- or amenorrhoea)
- Hyperandrogenism (biochemical or clinical)
- Polycystic ovaries (≥12) or ovarian volume >10cm^3 on USS

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61
Q

PCOS
What hormone tests may be used in PCOS?

A
  • Testosterone (raised)
  • SHBG (low)
  • LH (raised) + raised LH:FSH ratio (LH>FSH)
  • Prolactin (normal), TFTs (exclude causes)
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62
Q

PCOS
What other investigation may be useful at indicating PCOS?

A

2h 75g OTT for DM –
- IFG = 6.1–6.9mmol/L
- IGT (at 2h) = 7.8–11.1
- Diabetes (at 2h) = >11.1

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63
Q

PCOS
What is the gold standard for visualising the ovaries?
What might it show?

A
  • TVS
  • “String of pearls” appearance where follicles arranged around periphery of ovary (≥12 cysts or >10cm^3 ovarian volume)
  • Can also visualise endometrial thickness
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64
Q

PCOS
What are some associations and complications of PCOS?

A
  • DM, CVD + hypercholesterolaemia
  • Obstructive sleep apnoea, MH issues, sexual problems
  • Endometrial hyperplasia or cancer
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65
Q

PCOS
Why does PCOS increase risk of endometrial hyperplasia + cancer?

A
  • Oligo/anovulation means endometrial lining continues proliferating with unopposed oestrogen as no corpus luteum releasing progesterone
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66
Q

PCOS
What is the most crucial part of PCOS management?

A
  • Weight loss as can improve overall condition
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67
Q

PCOS
How is the risks of obesity, T2DM, CVD etc. managed in PCOS?

A
  • Lifestyle > diet + exercise, weight loss to reduce insulin resistance, smoking cessation
  • Orlistat (lipase inhibitor that stops fat absorption in intestines) may be given to assist weight loss if BMI >30kg/^m2
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68
Q

PCOS
What are the PCOS risk factors for endometrial cancer?
How is the risk of endometrial cancer managed in PCOS?

A
  • Obesity, DM, insulin resistance, amenorrhoea
  • Mirena coil for continuous endometrial protection
  • Induce withdrawal bleed AT LEAST every 3m with COCP or cyclical progesterones medroxyprogesterone 10mg 14d)
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69
Q

PCOS
How is infertility managed in PCOS?

A
  • Weight loss initial step to restore regular ovulation
  • Clomiphene to induce ovulation
  • Metformin may help (+ helps insulin resistance)
  • Laparoscopic ovarian drilling or IVF last resort
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70
Q

PCOS
How is hirsutism + acne managed?

A
  • Hair removal cream, topical eflornithine to treat facial hirsutism
  • Co-cyprindiol is COCP licensed for hirsutism + acne as anti-androgen effect but only used for 3m as increased VTE risk
  • Spironolactone by specialist (mineralocorticoid antagonist with anti-androgen effects)
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71
Q

CERVICAL CANCER
What is cervical cancer?

A
  • Most common cancer in women <35
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72
Q

CERVICAL CANCER
What has a strong association with development of cervical cancer?

A
  • Human papillomavirus (HPV) types 16 + 18 primarily a STI
  • Also associated with anal, vulval, vaginal, penis, mouth + throat cancers
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73
Q

CERVICAL CANCER
What genes may be implicated in cervical cancer?

A
  • P53 + pRb are tumour suppressor genes
  • HPV produces two oncoproteins (E6 + E7)
  • E6 inhibits P53, E7 inhibits pRB
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74
Q

CERVICAL CANCER
What are some risk factors for cervical cancer?

A
  • Increased risk of catching HPV = early (unsafe) sex, lots of sexual partners
  • Smoking (limits availability to clear HPV)
  • HIV
  • COCP
  • High parity
  • Previous CIN/abnormal smear or FHx
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75
Q

CERVICAL CANCER
How does cervical cancer present?

A
  • Asymptomatic + smear detected
  • Abnormal PV bleeding (POSTCOITAL, intermenstrual or postmenopausal)
  • PV discharge, pelvic pain, dyspareunia
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76
Q

CERVICAL CANCER
How would advanced cervical cancer present?

A
  • Menorrhagia
  • Ureteric obstruction
  • Weight loss
  • Bowel disturbance
  • Vesico-vaginal fistula
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77
Q

CERVICAL CANCER
What are some initial investigations for cervical cancer?

A
  • Speculum + swabs to exclude infection
  • Abnormal cervix (ulcerated, inflamed, bleeding, visible tumour) = urgent referral for colposcopy
  • Bimanual = rough + hard cervix
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78
Q

CERVICAL CANCER
How would you confirm a diagnosis of cervical cancer?

A

Colposcopy –
- Acetic acid causes abnormal cells to appear white “acetowhite”
- Schiller’s iodine test = healthy cells stain brown, abnormal do not stain
- Punch biopsy or large loop excision of transformation zone (LLETZ) for histology

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79
Q

CERVICAL CANCER
How is cervical cancer staged?

A

FIGO staging –
- 1 = confined to cervix
- 2 = invades uterus or upper 2/3 vagina
- 3 = invades pelvic wall (e.g. ureter) or lower 1/3 vagina
- 4 = invades beyond pelvis

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80
Q

CERVICAL CANCER
What is the cervical cancer screening?

A
  • Sexually active women 25–64 (triennially 25–50, 5y 50–64) smear test
  • Exceptions = HIV pts screened annually, women with previous CIN may require additional tests
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81
Q

CERVICAL CANCER
What is the process of cervical smears?

A
  • Smear test where cells collected from cervix + placed in preservation fluid for microscopy
  • Aims to identify precancerous changes (dyskaryosis) in epithelial cells of cervix for early treatment
  • Samples initially tested for high-risk HPV before examined
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82
Q

CERVICAL CANCER
What is dyskaryosis?
What results would warrant investigating?

A
  • Abnormal nucleus in cell
  • Borderline/mild = test sample for HPV (-ve = routine recall, +ve = normal 6w colposcopy referral)
  • Moderate = consistent with CIN II (urgent 2w colposcopy)
  • Severe = consistent with CIN III (urgent 2w colposcopy)
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83
Q

CERVICAL CANCER
How do you manage smear results?

A
  • Repeat inadequate smears within 3m or after 2 consecutive refer for colposcopy
  • HPV +ve but normal cytology = 12m, if +ve, 12m, if +ve at 24m > colposcopy (if HPV -ve then normal recall)
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84
Q

CERVICAL CANCER
What is used to grade the level of dysplasia, or premalignant change, in the cells of the cervix after colposcopy?

A
  • Cervical intra-epithelial neoplasia (CIN)
  • CIN I = mild, affects 1/3 thickness of epithelial layer, likely to return to normal without Tx
  • CIN II = mod, affects 2/3 thickness of epithelial layer, likely to progress to cancer without Tx
  • CIN III or cervical carcinoma in situ = severe, v likely to progress to cancer without Tx
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85
Q

CERVICAL CANCER
After treatment for CIN, when do patients have screening?

A
  • Screening at 6m for test of cure
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86
Q

CERVICAL CANCER
What is the prophylaxis for cervical cancer?

A
  • Children 12–13 HPV vaccine (6+11 genital warts, 16+18 cervical cancer)
  • Cervical screening
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87
Q

CERVICAL CANCER
What is the management of…

i) CIN or early stage 1A cervical cancer?
ii) Stage 1B-2A
iii) Stage 2B-4A
iv) Stage 4B

A

i) LLETZ or cone biopsy with -ve margins (maintain fertility)
ii) Radical hysterectomy + removal of pelvic LN with chemo (cisplatin) + radiotherapy
iii) Chemo + radiotherapy
iv) Combination of surgery, chemo/radio + palliative care

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88
Q

CERVICAL CANCER
What is the difference between LLETZ and cone biopsy?

A
  • LLETZ = LA during colposcopy, loop of wire with electrical current to cauterise tissue
  • Cone = GA where cone-shaped piece of cervix removed with scalpel
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89
Q

CERVICAL CANCER
What are the side effects of LLETZ and cone biopsy?

A
  • Bleeding + abnormal discharge weeks after, intercourse + tampon avoided as infection risk, may increase preterm labour
  • Pain, bleeding, infection, increased risk of premature labour + miscarriage
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90
Q

OVARIAN CANCER
What is ovarian cancer?
When do patients present?

A
  • Cancer of ovaries, usually presents late as non-specific Sx > worse prognosis
  • ≥70% present after spread beyond pelvis (most commonly para-aortic LN + liver)
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91
Q

OVARIAN CANCER
What are the 4 types of ovarian cancer?

A
  • Epithelial cell tumours (85–90%)
  • Germ cell tumours (common in women <35)
  • Sex cord-stromal tumours (rare)
  • Metastatic tumours
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92
Q

OVARIAN CANCER
What are some types of epithelial cell tumours?

A
  • Serous carcinoma (#1)
  • Endometrioid, clear cell, mucinous + undifferentiated tumours too
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93
Q

OVARIAN CANCER
What are germ cell tumours?

A
  • Often benign teratomas containing various tissue types like skin, teeth, hair
  • Rokitansky’s protuberance
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94
Q

OVARIAN CANCER
What are sex-cord stromal tumours?

A
  • Arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles)
  • Sertoli-Leydig + granulosa cell tumours
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95
Q

OVARIAN CANCER
What are metastatic tumours?

A
  • Secondary tumours
  • Krukenberg = metastasis in ovary, usually from GI (stomach) > CLASSIC “SIGNET-RING” CELLS ON HISTOLOGY
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96
Q

OVARIAN CANCER
What are some risk factors of ovarian cancer?

A

Unopposed oestrogen + increased # of ovulations –
- Early menarche
- Late menopause
- Increased age
- Endometriosis
- Obesity + smoking
Genetics (BRCA1/2, HNPCC/lynch syndrome)

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97
Q

OVARIAN CANCER
Hence, what are some protective factors of ovarian cancer?

A
  • COCP
  • Early menopause
  • Breast feeding
  • Childbearing
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98
Q

OVARIAN CANCER
How does ovarian cancer present?

A
  • Abdo pain, discomfort + bloating (IBS like)
  • Early satiety or loss of appetite
  • Urinary Sx as pressure on bladder (freq, urgency)
  • Change in bowel habit (obstruction later)
  • Abdo or pelvic mass, ascites
  • Germ cell = rapidly enlarging abdo mass (often causes rupture or torsion)
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99
Q

OVARIAN CANCER
What warrants a 2ww gynae oncology referral?

A
  • Ascites
  • Abdo or pelvic mass (unless clearly fibroids)
  • ≥250 risk of malignancy index score
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100
Q

OVARIAN CANCER
How is the risk of malignancy index calculated?

A
  • Menopausal status = 1 (pre) or 3 (post)
  • Pelvic USS findings = 1 (1 feature) or 3 (>1 feature)
  • CA-125 levels IU/mL as marker for epithelial cell ovarian cancer
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101
Q

OVARIAN CANCER
What are concerning pelvic USS findings?

A
  • Ascites
  • Metastases
  • Bilateral lesions
  • Solid areas
  • Multi-locular cysts
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102
Q

OVARIAN CANCER
What can cause falsely elevated CA-125 levels?

A
  • Endometriosis
  • Fibroids + adenomyosis
  • Pelvic infection
  • Pregnancy
  • Benign cysts
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103
Q

OVARIAN CANCER
What other investigations should be performed in ovarian cancer?

A
  • CT CAP for Dx + staging
  • Biopsy for histology
  • Paracentesis if ascites to test ascitic fluid for cancer cells
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104
Q

OVARIAN CANCER
What staging is used in ovarian cancer?

A

FIGO staging –
- 1 = confined to ovary
- 2 = past ovary but contained to pelvis
- 3 = past pelvis but inside abdomen (can be microscopically in lining of abdomen)
- 4 = spread to other organs

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105
Q

OVARIAN CANCER
What is the management of ovarian cancer?

A
  • Abdominal hysterectomy + bilateral salpingo-oopherectomy
  • May need bowel resections + chemo
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106
Q

OVARIAN CYST
What is a cyst?

A
  • Fluid-filled sac
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107
Q

OVARIAN CYST
What are the 4 types of ovarian cysts?

A
  • Functional (physiological)
  • Benign epithelial neoplasms
  • Benign germ cell neoplasms
  • Benign sex-cord stromal neoplasms
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108
Q

OVARIAN CYST
What are functional cysts?
Who are they seen in?
How do they present

A
  • Cysts relating to fluctuating hormones in the menstrual cycle
  • Pre-menopause, COCP is protective (inhibits ovulation)
  • Simple cysts = 2-3cm (can be up to 10cm), clear serous liquid, smooth internal lining, thin walls
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109
Q

OVARIAN CYST
What are the three types of functional cysts?

A
  • Follicular (most common)
  • Corpus luteum
  • Theca lutein
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110
Q

OVARIAN CYST
What are follicular cysts?
How is it managed?

A
  • Non-rupture of dominant follicle or failure of atresia > growth
  • Commonly regress after several cycles
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111
Q

OVARIAN CYST
What are corpus luteum cysts?
When are they seen?

A
  • Corpus luteum fails to breakdown, may fill with fluid or blood
  • May burst causing intraperitoneal bleeding
  • Early pregnancy
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112
Q

OVARIAN CYST
What are theca lutein cysts?
Association?

A
  • Stimulates growth of follicular theca cells so usually bilateral as resting follicles on both sides
  • Overstimulation of hCG (multiple + molar pregnancy as hCG v high)
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113
Q

OVARIAN CYST
What are some features of neoplastic cysts?

A
  • Often complex
  • > 10cm
  • Irregular borders
  • Internal septations appearing multi-locular
  • Heterogenous fluid
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114
Q

OVARIAN CYST
What are the 2 benign epithelial neoplasms?

A
  • Serous cystadenoma (most common epithelial tumour)
  • Mucinous cystadenoma
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115
Q

OVARIAN CYST
How does serous cystadenoma present?

A
  • May be bilateral, filled with watery fluid, 30–50y
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116
Q

OVARIAN CYST
How does mucinous cystadenoma present?

A
  • Often very large + contain mucus-like fluid
  • Pseudomyxoma peritonei where abdo cavity fills with gelatinous mucin secretions if rupture
  • 30–40y
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117
Q

OVARIAN CYST
What are benign germ cell neoplasms?

A
  • Dermoid cysts or teratomas
  • Common in women <35
  • May contain various tissue types (skin, teeth, hair + bone)
  • Can be bilateral, associated with ovarian torsion as heavy
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118
Q

OVARIAN CYST
What is an example of sex cord-stromal neoplasms?

A
  • Fibromas (small, solid benign fibrous tissue tumour)
  • Associated with Meig’s syndrome
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119
Q

OVARIAN CYST
What are some risk factors of ovarian cysts?

A
  • Obesity, tamoxifen, early menarche, infertility
  • Dermoid cysts = most common in young women, can run in families
  • Epithelial cysts = most common in post-menopausal (?malignant)
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120
Q

OVARIAN CYST
What is the clinical presentation of ovarian cyst?

A
  • Unilateral dull pelvic ache + may have dyspareunia
  • Pressure effects (frequent urination or bowel movements)
  • Abdo swelling or mass (ascites suggests malignancy, ruptured mucinous cystadenoma or Meig’s syndrome)
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121
Q

OVARIAN CYST
What is Meig’s syndrome?
Who is it commonly seen in?
What is the management?

A
  • Triad of fibroma, pleural effusion + ascites
  • Older women
  • Removal of fibroma = complete solution
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122
Q

OVARIAN CYST
What clinical presentation would suggest ovarian cyst rupture?

A
  • Acute, sharp abdo/pelvic pain
  • PV bleed, N+V (esp. torsion)
  • Shoulder tip pain if referred diaphragmatic pain
  • If peritonitis + shock occurs (fever, syncope, low BP, high HR)
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123
Q

OVARIAN CYST
What investigations should be done for ovarian cysts?

A
  • Beta-hCG to exclude uterine or ectopic
  • FBC for infection or haemorrhage
  • CA-125 if >40
  • Germ cell tumour markers if <40 with complex ovarian mass
  • Imaging (TVS or MRI abdo if larger mass)
  • Diagnostic laparoscopy (gold standard in ruptured cyst)
  • May need USS guided aspiration + cytology to confirm benign
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124
Q

OVARIAN CYST
What are the germ cell tumour markers?

A
  • Lactate dehydrogenase
  • Alpha-fetoprotein
  • Human chorionic gonadotropin
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125
Q

OVARIAN CYST
What are some complications of ovarian cysts?

A
  • Torsion leading to ovarian ischaemia = pain may be intermittent if untwists or stop if necrotic
  • Haemorrhage into cyst = sudden increase in size + pain (follicular + corpus luteal cysts)
  • Rupture of contents into peritoneum = peritonitis (associated with sex)
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126
Q

OVARIAN CYST
What is the management of a ruptured ovarian cyst?

A
  • ABCDE approach + admission
  • Stable = analgesia, fluids
  • Unstable or bleeding = surgery (?laparotomy)
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127
Q

OVARIAN CYST
What is the management of simple cysts in pre-menopausal women?

A
  • Small <5cm = likely to resolve within 3 cycles, no follow up
  • Mod 5–7cm = routine gynae referral + yearly USS
  • Large >7cm = ?MRI + surgical evaluation
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128
Q

OVARIAN CYST
What is the management of post-menopausal women presenting with an ovarian cyst?

A
  • Risk of malignancy index calculation
  • Simple cysts <5cm + normal CA-125 = monitor with 4–6m USS
  • Complex cyst or raised CA-125 = 2ww gynae oncology referral
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129
Q

OVARIAN CYST
What is the surgical management of ovarian cysts?
What are the indications?
What are the cautions?

A
  • Laparoscopic ovarian cystectomy ±oophorectomy
  • Persistent or enlarging cysts, Sx, ovarian torsion or Sx of rupture
  • Caution of chemical peritonitis with dermoid cysts if contents spill
130
Q

OVARIAN TORSION
What is ovarian torsion?

A
  • Ovary twists in relation to surrounding connective tissue, fallopian tube + blood supply (adnexa) leading to ischaemia ± necrosis if persists
131
Q

OVARIAN TORSION
What are some risk factors of ovarian torsion?

A
  • Pregnancy
  • Ovarian tumours/cysts
  • Previous surgery
  • Reproductive age
132
Q

OVARIAN TORSION
What is the clinical presentation of ovarian torsion?

A
  • Sudden onset, severe unilateral iliac fossa pain
  • Colicky if twists/untwists
  • May occur during exercise
  • N+V
  • Fever + pain stopping may indicate necrotic ovary
133
Q

OVARIAN TORSION
What are the investigations for ovarian torsion?

A
  • Localised tenderness ± palpable mass in pelvis
  • Beta-hCG to exclude ectopic
  • USS with colour doppler
134
Q

OVARIAN TORSION
What might USS show in ovarian torsion?

A
  • Free fluid in pelvis + oedema of ovary
  • “Whirlpool sign” = wrapping of vessels around central axis
  • Doppler studies may show lack of blood flow
135
Q

OVARIAN TORSION
What are some complications of ovarian torsion?

A
  • Delay in treatment may lead to loss of function > infertility or menopause if other ovary non-functional
  • Necrotic ovary may become infected > abscess > sepsis (or rupture causing peritonitis + adhesions)
136
Q

OVARIAN TORSION
What is the management of ovarian torsion?

A
  • Laparoscopy for definitive diagnosis + treatment
  • Untwist ovary + fix into place (detorsion)
  • Oophorectomy based on visual appearance (necrotic)
  • Analgesia + fluid resus
137
Q

ENDOMETRIAL CANCER
What is endometrial cancer?
What is the prognosis?

A
  • Cancer of endometrium (lining of uterus) = oestrogen dependent
  • 90% women are >50, good prognosis, 5-year survival in stage 1 = 80%
138
Q

ENDOMETRIAL CANCER
What is the most common histological type of endometrial cancer?
What are some others?

A
  • Adenocarcinoma (80%)
  • Adenosquamous, squamous, papillary serous, clear cell + uterine sarcoma
139
Q

ENDOMETRIAL CANCER
What are some risk factors for endometrial cancer?

A

Unopposed oestrogen –
- Obesity (adipose tissue contains aromatase)
- Nulliparous
- Early menarche
- Late menopause
- Oestrogen-only HRT
- Tamoxifen
- PCOS
- Increased age
- T2DM
- HNPCC (Lynch syndrome)

140
Q

ENDOMETRIAL CANCER
What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking (Seem to have anti-oestrogenic effect)
141
Q

ENDOMETRIAL CANCER
What is the clinical presentation of endometrial cancer?

A
  • PMB is endometrial cancer until proven otherwise
  • May have abnormal bleeding (PCB, IMB, menorrhagia)
  • Abnormal PV discharge + pain less commonly
142
Q

ENDOMETRIAL CANCER
What is the first line investigation for endometrial cancer?

A
  • TVS = endometrial thickness should be <4mm
  • Recommended for >55 w/ unexplained PV discharge + visible haematuria
143
Q

ENDOMETRIAL CANCER
What other investigations is recommended in endometrial cancer?

A
  • Pipelle biopsy via speculum (highly sensitive so useful for exclusion in low risk)
  • Hysteroscopy with endometrial biopsy
  • 2WW urgent gynae oncology referral if PMB in ≥55y
144
Q

ENDOMETRIAL CANCER
What is the staging for endometrial cancer?

A

FIGO staging –
- 1 = confined to endometrium + uterus
- 2 = tumour invaded cervix
- 3 = cancer spread to ovary, vagina, fallopian tubes or LN
- 4 = cancer invades bladder, rectum or beyond pelvis

145
Q

ENDOMETRIAL CANCER
What is the management of stage 1 + 2 endometrial cancer?

A
  • Total abdominal hysterectomy with bilateral salpingo-oopherectomy + pelvic LN
146
Q

ENDOMETRIAL CANCER
What other treatments are there for endometrial cancer?

A
  • Surgery = radical hysterectomy ± pelvic LN
  • Radiotherapy = adjuvant (brachytherapy/external beam)
  • Chemo, progesterone therapy to slow progression of cancer
148
Q

ENDOMETRIAL POLYP
What is an endometrial polyp?
What is the main differential?

A
  • Benign growths of endometrium, some may be (pre)cancerous
  • Fibroids
149
Q

ENDOMETRIAL POLYP
What are some risk factors of endometrial polyps?

A
  • Being peri or post-menopausal
  • HTN
  • Obesity
  • Tamoxifen
150
Q

ENDOMETRIAL POLYP
What is the clinical presentation of endometrial polyps?

A
  • Irregular menstrual bleeding (IMB, PMB), menorrhagia
  • Infertility in younger as competing with foetus for space
151
Q

ENDOMETRIAL POLYP
What are the investigations for endometrial polyps?

A
  • TVS/TAS
  • Hysteroscopy ± endometrial biopsy
152
Q

ENDOMETRIAL POLYP
What is the management of endometrial polyps?

A
  • Conservative but monitor or biopsy if concerns
  • GnRH analogues as oestrogen sensitive
  • If post-menopause or pre but symptomatic = hysteroscopic resection or morcellation of polyps
  • Hysterectomy if severe
153
Q

VULVAL CANCER
What is vulval cancer?
What is the most common histological type?

A
  • Rare compared to other cancers
  • Squamous cell carcinomas (90%), malignant melanoma less common
154
Q

VULVAL CANCER
What are some risk factors for vulval cancer?

A
  • Vulval intraepithelial neoplasia (VIN) due to HPV in younger women
  • Lichen sclerosus in older women
155
Q

VULVAL CANCER
What is the clinical presentation of vulval cancer?

A
  • Vulval itching, soreness + persistent lump on labia majora
  • Ulceration, bleeding, pain (sometimes on urination)
  • May be lymphadenopathy in groin
156
Q

VULVAL CANCER
What are the investigations for vulval cancer?

A
  • Suspected = 2ww urgent gynae oncology referral
  • Biopsy lesion with sentinel node biopsy to see if LN spread
157
Q

VULVAL CANCER
How is vulval cancer staged?

A

FIGO staging –
- 1 = <2cm
- 2 = >2cm
- 3 = adjuvant organs or unilateral nodes
- 4 = distant mets or bilateral nodes

158
Q

VULVAL CANCER
What is vulval intraepithelial neoplasia (VIN)?

A
  • Premalignant condition affecting squamous epithelium that can precede vulval cancer
159
Q

VULVAL CANCER
What are 2 types of VIN?

A
  • High grade squamous intraepithelial lesion = type of VIN associated with HPV typically in younger women 35–50
  • Differentiated VIN associated with lichen sclerosus
160
Q

VULVAL CANCER
What is the management of VIN?

A
  • Biopsy to Dx
  • Watch + wait with close follow up
  • Wide local excision to surgically remove lesion
  • Imiquimod cream or laser ablation
161
Q
A
161
Q

VULVAL CANCER
What is the management of vulval cancer?

A
  • Radical or conservative surgery (WLE ± groin LN dissection)
  • Radio ± chemotherapy
162
Q

VAGINAL CANCER
What is the most common histological type of vaginal cancer?

A
  • 90% squamous
163
Q

MENOPAUSE
What is menopause?

A
  • Permanent cessation of menstruation where ovarian activity ceases to function, can occur after TAH-BSO
164
Q

MENOPAUSE
What is perimenopause?

A
  • Time around menopause where woman may have vasomotor Sx + irregular periods
  • Includes time leading up to LMP + 12m after
165
Q

MENOPAUSE
What is the physiology of menopause?

A
  • Starts with decline in development of ovarian follicles
  • Less oestrogen + progesterone production
  • Absence of -ve feedback loop so FSH + LH rises
  • Falling follicular development = anovulation so irregular menstrual cycles
  • Low oestrogen = endometrium does not develop so amenorrhoea + perimenopausal Sx
166
Q

MENOPAUSE
What are the peri-menopausal symptoms?

A
  • Vasomotor = hot flushes, night sweats, impact on QOL
  • General = mood swings, decreased libido, vaginal dryness, headache, dry skin, loss of energy, joint aches, muscles pains, irregular periods
167
Q

MENOPAUSE
What are some medium-term presentations of menopause?

A
  • Urogenital atrophy leading to dyspareunia, recurrent UTIs + PMB
168
Q

MENOPAUSE
Why does urogenital atrophy occur?

A
  • Urogenital tract has oestrogen receptors + continual stimulation keep it strong + supple
169
Q

MENOPAUSE
What are the investigations for menopause?

A
  • Retrospective diagnosis after 12m of amenorrhoea in women >45y
  • NICE recommends FSH (high) blood test in women <40 with suspected premature menopause or women 40–45 with menopausal Sx or change in menstrual cycle
170
Q

MENOPAUSE
What are the long-term complications of menopause?

A
  • Osteoporosis as oestrogen inhibits osteoclasts + can become hyperactive
  • CVD, stroke (esp. in early menopause) + dementia
171
Q

MENOPAUSE
When is contraception recommended in relation menopause?
Why?

A
  • 2y after LMP in <50, 1y after LMP in >50
  • Pregnancy >40 has increased risks + complications
172
Q

MENOPAUSE
What contraception is suitable in older women?
How do hormonal contraceptives affect the menopause?

A
  • UKMEC1 = barrier, IUS/IUD, POP, long-acting progesterone (<45), sterilisation
  • UKMEC2 = COCP after 40 used until 50, try ones with levonorgestrel or norethisterone as lower VTE risk
  • They don’t but may mask Sx
173
Q

MENOPAUSE
What is the initial management of menopause?

A

Lifestyle –
- Vasomotor symptoms last 2-5y without intervention so ?no treatment
- Regular exercise can improve hot flushes, mood + cognitive Sx
- Good sleep hygiene can improve sleep disturbance

174
Q

MENOPAUSE
What is the management of menopause in more severe cases?

A
  • HRT first-line for vaso-motor Sx as most effective
  • Clonidine (alpha adrenergic receptor agonist) second line with low-dose antidepressants like venlafaxine (not C/I in breast cancer Tx) or fluoxetine
  • CBT
  • Vaginal oestrogen cream/tablets + moisturisers for dryness
175
Q

MENOPAUSE
What is the mechanism of action of clonidine?

A
  • Alpha-adrenergic receptor agonist
176
Q

HRT
What is Hormone Replacement Therapy (HRT)?
How does this compare to the COCP?

A
  • Treatment to alleviate Sx associated with menopause by giving physiological dose of oestrogen as replacement for what body is used to
  • COCP gives a supraphysiological dose of oestrogen
177
Q

HRT
What are some indications for HRT?

A
  • Replacing hormones in POI even without Sx
  • Reducing vasomotor + other Sx in menopause
  • Reduce osteoporosis risk in women <60
178
Q

HRT
What are some benefits of HRT?

A
  • Improved Sx control
  • Improved QOL
  • Reduced risk of osteoporosis
179
Q

HRT
What are some risks with HRT?

A
  • Increased risk of breast cancer by adding progesterone
  • Increased risk of endometrial cancer by oestrogen alone
  • Increased risk of VTE
  • Increased risk of stroke + IHD
180
Q

HRT
How can the HRT risks be managed for…

i) breast cancer?
ii) endometrial cancer?
iii) VTE?
iv) IHD?

A

i) Local (Mirena) instead of systemic progesterones, risk declines after 5y stopping
ii) Add progesterone (esp Mirena) to prevent endometrial hyperplasia
iii) Transdermal patch
iv) Do not take for >10y after menopause

181
Q

HRT
What are some contraindications to HRT?

A
  • Undiagnosed PV bleeding
  • Current or past breast cancer
  • Any oestrogen sensitive cancer (endometrial)
182
Q

HRT
What HRT would you give to…

i) woman without uterus?
ii) woman with uterus?
iii) woman with period within past 12m?
iv) woman with period >12m ago?

A

i) Continuous oestrogen-only HRT
ii) Add progesterone (combined HRT)
iii) Cyclical combined HRT
iv) Continuous combined HRT

183
Q

HRT
What preparations of HRT are there?

A
  • Pessary + cream (local Sx like bleeding, pain, UTI), transdermal patch, tablets
  • Tibolone is a synthetic steroid hormone that acts as continuous combined (only used >12m from LMP)
184
Q

HRT
When would patches be used for HRT?
What is the most common side effect?

A
  • Pt choice
  • GI upset (Crohn’s)
  • VTE risk
  • Co-morbidities like HTN
  • Skin irritation #1
185
Q

HRT
How can oestrogen be given?

A
  • Tablets or transdermal (patches or gels)
186
Q

HRT
When would you use cyclical progesterone compared to continuous?

A
  • Perimenopausal women to allow monthly breakthrough bleed during oestrogen-only part of cycle (10–14d/month)
  • Continuous after amenorrhoeic for 2y <50 or 1y >50 as before this can cause irregular breakthrough bleeding
  • After 12m of treatment can switch to continuous
187
Q

HRT
How can progesterone be given?

A
  • Tablets, transdermal (patches) or IUS (Mirena)
188
Q

HRT
What would you give for…

i) cyclical combined HRT?
ii) continuous HRT?

A

i) Sequential tablets or patches
ii) Mirena licensed for 4 years for endometrial protection – also treats menorrhagia

189
Q

HRT
What are the side effects associated with oestrogen?

A
  • Nausea,
  • bloating,
  • headaches,
  • breast swelling or tenderness,
  • leg cramps
190
Q

ATROPHIC VAGINITIS
What is atrophic vaginitis?

A
  • Dryness + atrophy of vaginal mucosa related to lack of oestrogen
191
Q

ATROPHIC VAGINITIS
What is the pathophysiology of atrophic vaginitis?

A
  • Epithelial lining of vagina + urinary tract responds to oestrogen by becoming thicker, more elastic + producing secretions so reduced oestrogen has opposite effect
  • Tissue more prone to inflammation + changes in vaginal pH + microbial flora that contribute to localised infections
192
Q

ATROPHIC VAGINITIS
What are some risk factors for atrophic vaginitis?

A
  • Menopause
  • Oophorectomy
  • Anti-oestrogen (tamoxifen, anastrozole)
193
Q

ATROPHIC VAGINITIS
What is the clinical presentation of atrophic vaginitis?

A
  • Postmenopausal with PV dryness, dyspareunia + occasional spotting
  • Consider with recurrent UTIs, stress incontinence or pelvic organ prolapse
194
Q

ATROPHIC VAGINITIS
What might the PV examination show in atrophic vaginitis?

A
  • Sparse pubic hair
  • Pale mucosa
  • Dryness
  • Thin skin
  • Reduced vaginal folds
  • May be painful
195
Q

ATROPHIC VAGINITIS
What is the management of atrophic vaginitis?

A
  • Vaginal lubricants + moisturisers like Sylk + Replens
  • Topical oestrogen like estriol cream, HRT if severe
196
Q

URINARY INCONTINENCE
What is urinary incontinence?

A
  • Involuntary leakage of urine at socially unacceptable times
  • Affects 20% of adult women
197
Q

URINARY INCONTINENCE
What is the physiology of micturition?

A
  • Detrusor = smooth muscle, transitional epithelium normally only contracts during micturition = sacral parasympathetic innervation from S2-4
  • M2+3 muscarinic receptors with ACh
  • Sympathetic nerve fibres from T11-L2 maintain relaxation of bladder for storage
198
Q

URINARY INCONTINENCE
What are the 6 main types of incontinence?

A
  • Overactive bladder/urge incontinence
  • Stress incontinence
  • Mixed incontinence (of the 2 above)
  • Overflow incontinence
  • Fistula
  • Neurological
199
Q

URINARY INCONTINENCE
What causes urge incontinence/OAB?

A
  • Overactivity + involuntary contractions of the detrusor muscle
200
Q

URINARY INCONTINENCE
What is the pathophysiology of stress incontinence?

A
  • Weakness of pelvic floor + sphincter muscles
  • Detrusor pressure > closing pressure of urethra
201
Q

URINARY INCONTINENCE
What is overflow incontinence?

A
  • Chronic urinary retention due to outflow obstruction leads to overflow of urine + incontinence without the urge to pass, M>F
202
Q

URINARY INCONTINENCE
What are some causes of overflow incontinence?

A
  • Anticholinergics
  • Fibroids
  • Pelvic tumours
  • BPH (men)
  • Neuro (damage, MS, diabetic neuropathy, spinal cord injuries)
203
Q

URINARY INCONTINENCE
How does neurology cause incontinence?

A

Nerve damage, MS or functional

204
Q

URINARY INCONTINENCE
What are some risk factors for urinary incontinence?

A
  • Increasing age
  • Multiparity
  • High BMI
  • FHx
  • Previous pelvic surgery (hysterectomy)
205
Q

URINARY INCONTINENCE
What is the clinical presentation of urge incontinence/OAB?

A
  • Urgency, frequency, nocturia
  • ‘Key in door’ + ‘handwash’ trigger bladder contractions
  • Intercourse
  • May affect activities + QOL as worried about toilet access
206
Q

URINARY INCONTINENCE
What is the clinical presentation of stress incontinence?

A
  • Involuntary leakage when increased pressure (cough, laugh, lifting, exercise)
207
Q

URINARY INCONTINENCE
What are some investigations in urinary incontinence?

A
  • Hx most important
  • Bladder diary (frequency volume chart) first line
  • Urine dipstick + MSU
  • Residual urine measurement
  • Electronic Personal Assessment Questionnaire
  • Urodynamics
  • Cystogram with contrast
208
Q

URINARY INCONTINENCE
What does a bladder diary look at?

A
  • Frequency + quantity of both urination and leakage
  • Fluid intake + diurnal variation
209
Q

URINARY INCONTINENCE
What are you looking for in urine dipstick + MSU?

A
  • Nitrites + leukocytes = infection
  • Microscopic haematuria = glomerulonephritis
  • Proteinuria = renal disease
  • Glycosuria = DM, nephropathy
210
Q

URINARY INCONTINENCE
How do you measure residual urine?

A
  • In/out catheter or USS
211
Q

URINARY INCONTINENCE
What is the Electronic Personal Assessment Questionnaire (ePAQ)?

A

Determines impact on QOL + assesses –
- Urinary (pain, voiding, stress, OAB, QOL)
- Vaginal (pain, capacity, prolapse, QOL)
- Bowel (IBS, constipation, continence, QOL)
- Sexual (dyspareunia, overall sex life)

212
Q

URINARY INCONTINENCE
What is the purpose of urodynamics?

A

Measures pressure in abdomen + bladder to deduce detrusor pressure

213
Q

URINARY INCONTINENCE
What is some lifestyle advice for urinary incontinence?

A
  • Weight loss
  • Stop smoking
  • Reduce caffeine + alcohol
  • Avoid straining + constipation
214
Q

URINARY INCONTINENCE
What are some conservative treatments for urinary incontinence?

A
  • Leakage barriers (pads), skin care + odour control
  • Bladder bypass with urethral, suprapubic or intermittent self-catheters
  • PV oestrogen to reduce urinary Sx
215
Q

URINARY INCONTINENCE
What is the stepwise management of urge incontinence/OAB?

A
  • 1st line = bladder retraining (6w gradually increasing time between voiding)
  • 1st line drugs = anti-muscarinics (oxybutynin, tolterodine, darifenacin)
  • Mirabegron (beta-3-adrenergic agonist) if anti-muscarinics not tolerated
216
Q

URINARY INCONTINENCE
What is the mechanism of action of anti-muscarinics?

A
  • Parasympathetic so Pissing = decreases need to urinate + spasms
217
Q

URINARY INCONTINENCE
What is the mechanism of action of beta-3-adrenergic agonists?

A
  • Sympathetic so Storage = relaxes detrusor + increases bladder capacity
218
Q

URINARY INCONTINENCE
What are last resort options for urge incontinence?

A
  • Augmentation cystoplasty with bowel tissue
  • Bypass (urostomy)
  • Botox can paralyse detrusor + block ACh release
219
Q

URINARY INCONTINENCE
What is the first line management of stress incontinence?

A
  • Pelvic floor exercises with physio for 3m
  • Pelvic floor muscle contraction > clamping of urethra > increased urethral pressure so reduced leakage
220
Q

URINARY INCONTINENCE
What medical management can be used in urinary incontinence?

A
  • Duloxetine (SNRI)
221
Q

URINARY INCONTINENCE
What are the surgical interventions for stress incontinence?

A
  • Colposuspension
  • Tension free vaginal tape (TVT)
  • Autologous sling procedures (TVT but strip of fascia from abdo wall)
222
Q

URINARY INCONTINENCE
What are the aims of surgical interventions of stress incontinence?

A
  • Restore pressure transmission to urethra
  • Support or elevate urethra (anterior wall + pubic symphysis stitches in colposuspension, mesh sling looping urethra in TVT)
  • Increase urethral resistance
223
Q

PELVIC ORGAN PROLAPSE
What is pelvic organ prolapse?

A
  • Descent of ≥1 pelvic organs resulting in protrusion on the vaginal walls
  • Due to weakness + stretching of ligaments + muscles surround uterus, rectum + bladder (levator ani + endopelvic fascia support pelvic organs)
224
Q

PELVIC ORGAN PROLAPSE
What are the 5 types of prolapse?

A
  • Cystocele
  • Rectocele
  • Enterocele
  • Uterine prolapse
  • Vault prolapse
225
Q

CYSTOCELE
What is a cystocele?

A
  • Defect in ant. vaginal wall = bladder prolapses backwards into vagina (can get urethrocele or cystourethrocele)
226
Q

RECTOCELE
What is a rectocele?

A
  • Defect in post. vaginal wall = rectum prolapses forwards into vagina
227
Q

PELVIC ORGAN PROLAPSE
What is an enterocele?

A

Defect in upper posterior wall of vagina > intestine protrusion

228
Q

PELVIC ORGAN PROLAPSE
What are some risk factors of pelvic organ prolapse?

A
  • Age
  • BMI
  • Multiparity (vaginal)
  • Spina bifida
  • Pelvic surgery
  • Menopause
229
Q

CYSTOCELE
What is the clinical presentation of a cystocele?

A
  • “Something coming down” = dragging/heavy sensation in pelvis
  • Pain, lump, discomfort
  • incontinence, urgency, frequency, poor stream + retention
  • Sexual dysfunction = pain, altered sensation + reduced enjoyment
230
Q

PELVIC ORGAN PROLAPSE
What are the investigations for pelvic organ prolapse?

A
  • Sim’s speculum (U-shaped) to show if something is there
  • May have urodynamics, USS or MRI
231
Q

PELVIC ORGAN PROLAPSE
What is the management for pelvic organ prolapse?

A
  • Conservative = pelvic floor exercises, weight loss + diet changes
  • Vaginal pessary = ring (preferred as can have sex), shelf or Gellhorn
  • Surgery (symptomatic or severe like outside vagina, ulcerated, failed Mx)
232
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for cystocele/cystourethrocele?

A

Anterior colporrhaphy or colposuspension

233
Q

PREMENSTRUAL SYNDROME
What is premenstrual syndrome (PMS)?

A
  • Psychological, emotional + physical Sx that occur prior to menstruation
234
Q

PREMENSTRUAL SYNDROME
What is thought to cause PMS?

A
  • Fluctuation in oestrogen + progesterone during the cycle
235
Q

PREMENSTRUAL SYNDROME
How may PMS present?

A
  • Mood = anxiety, swings, stress, fatigue, low confidence
  • Physical = bloating, headaches, breast pain
  • Resolves on menstruation
  • Absent before menarche, during pregnancy or after menopause
236
Q

PREMENSTRUAL SYNDROME
How is PMS diagnosed?

A
  • Sx diary spanning 2 menstrual cycles
  • Definitive Dx with GnRH to temporarily induce menopause = Sx resolve
237
Q

PREMENSTRUAL SYNDROME
What is the conservative management of PMS?

A
  • Healthy diet, exercise, alcohol + smoking cessation, stress reduction, good sleep patterns
238
Q

PREMENSTRUAL SYNDROME
What management can be trialled in primary care for PMS?

A
  • SSRIs
  • COCP
  • CBT
239
Q

PREMENSTRUAL SYNDROME
What specialist management can be given for PMS?

A
  • Continuous transdermal oestrogen with progestogens
  • GnRH analogues if severe (add HRT to mitigate osteoporosis risk)
  • Hysterectomy + bilateral oophorectomy to induce menopause if severe
  • Danazol + tamoxifen for cyclical breast pain
  • Spironolactone for breast swelling + bloating
240
Q

DYSMENORRHOEA
What is dysmenorrhoea?

A
  • Painful menstruation ± N+V
241
Q

DYSMENORRHOEA
What is primary dysmenorrhoea?

A

No underlying pathology, may be due to excessive endometrial prostaglandins – presents as suprapubic cramps just before or within few hours of period starting

242
Q

DYSMENORRHOEA
What is the management of primary dysmenorrhoea?

A
  • NSAIDs like mefenamic acid during menstruation
  • COCP second line
243
Q

AIS
What is androgen insensitivity syndrome (AIS)?

A
  • X-linked recessive condition (androgen receptor gene mutation) with end-organ resistance to testosterone causing male genotype 46XY but female phenotype
244
Q

AIS
What is the pathophysiology of AIS?

A
  • Absent response to testosterone + conversion of additional androgens to oestrogen result in female secondary sexual characteristics
  • Typical male sexual characteristics (Wollfian structures) do not develop
245
Q

AIS
What is the clinical presentation of AIS?

A
  • Infancy = inguinal hernias with undescended testes
  • Puberty = primary amenorrhoea + infertile
  • Tend to be taller than average, lack of pubic + facial hair as well as male muscle development
  • Female external genitalia (but not internal) + breasts
246
Q

AIS
Why is their female external genitalia but not internal in AIS?

A
  • Undescended testes in abdo or inguinal canal produce AMH which prevents uterus, upper vagina, tubes + ovaries developing (Mullerian duct structures)
247
Q

AIS
What is the clinical presentation of partial AIS?

A
  • More ambiguous
  • Micropenis
  • Clitoromegaly
  • Bifid scrotum
  • Hypospadias
  • Reduced male features
248
Q

AIS
What are the investigations for AIS?

A

Hormone tests show raised –
- LH
- FSH (or normal)
- Testosterone (or normal for male)
- Oestrogen (for male)
Pelvic USS = absent female internal organs
Karyotyping = 46XY

249
Q

AIS
What is the management of AIS?

A
  • Specialist MDT (paeds, gynae, urology, endo, psychology)
  • Bilateral orchidectomy to avoid testicular cancer
  • Oestrogen therapy
  • Vaginal dilators or surgery to create adequate length
  • In general, raised as female but counselling for support
250
Q

ASHERMAN’S SYNDROME
What is Asherman’s syndrome?

A
  • Adhesion formation within uterus following damage
251
Q

ASHERMAN’S SYNDROME
What is the pathophysiology of Asherman’s?

A
  • Damage to basal layer of endometrium, damaged tissue may heal abnormally, creating scar tissue (adhesions)
  • Adhesions can bind uterine walls together or endocervix, sealing it shut causing obstruction > infertility, 2* amenorrhoea
252
Q

ASHERMAN’S SYNDROME
What causes Asherman’s syndrome?

A
  • Pregnancy-related dilatation + curettage procedures
  • After uterine surgery
  • Pelvic infection like endometritis
253
Q

ASHERMAN’S SYNDROME
What is the clinical presentation of Asherman’s syndrome?

A
  • Secondary amenorrhoea
  • Infertility
  • Significantly lighter periods
  • Dysmenorrhoea
254
Q

ASHERMAN’S SYNDROME
What is the management of Asherman’s syndrome?

A
  • Hysterosalpingography = contrast injected into uterus + XR
  • Sonohysterography = uterus filled with fluid + pelvic USS
  • Hysteroscopy gold standard + can dissect adhesions (recurrence after common)
255
Q

FIBROIDS
What are the issues with subserosal fibroids?

A

Grow outwards + can become very large, filling the abdominal cavity

256
Q

ENDOMETRIOSIS
What are some protective factors?

A

Multiparity + COCP

257
Q

CERVICAL CANCER
What is cervical cancer?
What is the histological type of cervical cancer?

A
  • Most common cancer in women <35
  • Squamous cell carcinoma 80%, then adenocarcinoma (small cell rare)
258
Q

VAGINAL CANCER
What is the management?

A

Intravaginal radiotherapy or sometimes radical surgery

259
Q

VAGINAL CANCER
What causes it?

A

HPV or metastatic spread from cervix or vulva

260
Q

VAGINAL CANCER
What is the prognosis like?

A

Poor prognosis, average survival at 5 years 50%

261
Q

VAGINAL CANCER
How does it present?

A

Bleeding or discharge, evident mass or ulcer

262
Q

MENOPAUSE
What is the average age of onset? When is it premature?

A

Average age = 51,
premature <40

263
Q

MENOPAUSE
What can urogenital atrophy lead to?

A

Urinary incontinence + pelvic organ prolapse

264
Q

HRT
What are the side effects associated with progesterone?

A

Mood swings,
fluid retention,
weight gain,
acne
greasy skin

265
Q

RECTOCELE
How may this present?

A
  • Faecal loading in that part of rectum may lead to lump in vagina + have to use finger to press lump to aid defecation
  • “Something coming down” = dragging/heavy sensation in pelvis
  • Pain, lump, discomfort
  • constipation, incontinence + urgency
  • Sexual dysfunction = pain, altered sensation + reduced enjoyment
266
Q

PELVIC ORGAN PROLAPSE
What is a vault prolapse?

A

If had total hysterectomy, top of vagina (vault) descends into the vagina

267
Q

PELVIC ORGAN PROLAPSE
What is a uterine prolapse?

A

Uterus descends into vagina

268
Q

PELVIC ORGAN PROLAPSE
What is the clinical presentation of pelvic organ prolapse?

A
  • “Something coming down” = dragging/heavy sensation in pelvis
  • Pain, lump, discomfort
  • Urinary Sx (cystocele) = incontinence, urgency, frequency, poor stream + retention
  • Bowel Sx (rectocele) = constipation, incontinence + urgency
  • Sexual dysfunction = pain, altered sensation + reduced enjoyment
269
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for uterine prolapse?

A

Hysterectomy or sacrohysteropexy

270
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for rectocele?

A

Posterior colporrhaphy

271
Q

DYSMENORRHOEA
What are the two types?

A

Primary + secondary

272
Q

HYDATIDIFORM MOLE
What is a hydatidiform mole?

A
  • Part of group of rare tumours known as gestational trophoblastic disease
  • Growing mass of tissue that implants into uterus that will not come to term (non-viable fertilised egg, result of abnormal conception)
273
Q

HYDATIDIFORM MOLE
What are the 3 types of hydatidiform mole?

A
  • Complete
  • Partial
  • Invasive
274
Q

HYDATIDIFORM MOLE
What is a complete mole?

A
  • Diploid trophoblast cells
  • Empty egg + sperm that duplicates DNA (all genetic material comes from father)
  • No foetal tissue
275
Q

HYDATIDIFORM MOLE
What is a partial mole?

A
  • Triploid (69XXX, 69XXY) trophoblast cells
  • 2 sperm fertilise 1 egg
  • Some recognisable foetal tissue
276
Q

HYDATIDIFORM MOLE
What is an invasive mole?
What is the significance of this?

A
  • When a complete mole invades the myometrium
  • Metaplastic potential to evolve into a choriocarcinoma
277
Q

HYDATIDIFORM MOLE
What are some risk factors for hydatidiform mole?

A
  • Extremes of reproductive age
  • Previous molar pregnancy
  • Multiple pregnancies
  • Asian women
  • OCP
278
Q

HYDATIDIFORM MOLE
What is the clinical presentation of hydatidiform mole?

A
  • PV bleed in first or early second trimester
  • Uterus bigger than expected for gestation
  • Severe hyperemesis
  • Early pre-eclampsia + clinical hyperthyroidism (hCG can mimic TSH)
279
Q

HYDATIDIFORM MOLE
What are some investigations for hydatidiform mole?

A
  • Serum beta-hCG abnormally high (trophoblastic tissue producing excessive amounts > hyperemesis + thyrotoxicosis)
  • USS shows snowstorm appearance
  • Dx confirmed with histology after evacuation
280
Q

HYDATIDIFORM MOLE
What is the main complication of hydatidiform mole?

A
  • 2-3% complete moles transition to highly malignant choriocarcinoma which can metastasise to the lungs
  • These are placental site trophoblastic tumours
281
Q

HYDATIDIFORM MOLE
What is the management for hydatidiform mole?

A
  • Urgent referral to specialist centre
  • Complete moles = suction dilation + curettage
  • Partial moles = suction or medical evacuation
  • Invasive = suction D+C but not all removed, some resolve
282
Q

HYDATIDIFORM MOLE
What is the management of hydatidiform mole after evacuation?

A
  • Check urinary pregnancy test in 3w – if high or mets may need chemo (cisplatin)
  • Effective contraception as advised to avoid pregnancy for 12m
283
Q

PELVIC INFLAMMATORY DISEASE
What is pelvic inflammatory disease?

A
  • Inflammation + infection of the pelvic organs (upper genital tract), caused by ascending infection through the cervix.
284
Q

PELVIC INFLAMMATORY DISEASE
What are the STI causes of PID?

A
  • N. gonorrhoea (tends to be more severe),
  • chlamydia trachomatis (most common),
  • Mycoplasma genitalium
285
Q

PELVIC INFLAMMATORY DISEASE
What are some risk factors for PID?

A
  • Not using barrier contraception
  • Multiple sexual partners
  • Intrauterine device
  • Younger age
  • Existing STIs
  • Previous PID
286
Q

PELVIC INFLAMMATORY DISEASE
What is the clinical presentation of PID?

A
  • Pelvic/lower abdo pain (chronic)
  • Abnormal PV discharge (purulent), urinary Sx (dysuria, frequency).
  • Abnormal bleeding (IMB, PCB, dysmenorrhoea).
  • Deep dyspareunia
  • Fever (± other signs of sepsis)
287
Q

PELVIC INFLAMMATORY DISEASE
What are some differentials of PID?

A
  • Appendicitis
  • Ectopic
288
Q

PELVIC INFLAMMATORY DISEASE
What might you find on a clinical examination in PID?

A
  • Pelvic/adnexal tenderness.
  • Cervical excitation (motion tenderness)
  • Cervicitis
  • Purulent discharge
289
Q

PELVIC INFLAMMATORY DISEASE
What investigations would you do in PID?

A
  • Pregnancy test to exclude ectopic
  • NAAT swabs for gonorrhoea + chlamydia
  • HVS for BV, candidiasis + trichomoniasis
  • HIV + syphilis bloods
  • FBC, blood cultures + CRP/ESR if acutely unwell/septic
  • TV USS if abscess suspected
290
Q

PID
What might you look for on microscopy in PID?
What is the relevance?

A
  • Pus cells on swabs from vagina or endocervix
  • Absence is useful to exclude PID
291
Q

PELVIC INFLAMMATORY DISEASE
What are the complications of PID?

A
  • Sepsis
  • Abscess
  • Subfertility from tubal blockage
  • Chronic pelvic pain
  • Ectopics
  • Fitz-Hugh-Curtis syndrome
292
Q

PELVIC INFLAMMATORY DISEASE
What is Fitz-Hugh-Curtis syndrome?
What does it cause?

A
  • Inflammation + infection of liver (Glisson’s) capsule.
  • Leads to adhesions between liver + peritoneum, bacteria may spread from pelvis via peritoneal cavity, lymphatics or blood
293
Q

PELVIC INFLAMMATORY DISEASE
What is the management of PID?

A
  • 1g stat IM ceftriaxone (gonorrhoea)
  • 100mg BD doxycycline for 14d (chlamydia + MG)
  • Metronidazole 400mg BD for 14d (Gardnerella)
  • GUM referral for specialist Mx + contact tracing
  • Hospital admission for IV Abx if signs of sepsis or pregnant
  • Pelvic abscess > drainage
294
Q

PELVIC INFLAMMATORY DISEASE
What organs can be infected?

A

Uterus - Endometritis
Fallopian tubes - salpingitis,
Ovaries - oophoritis,
Peritoneum - peritonitis,
Parametrium - parametritis (parametrium which is connective tissue around the uterus).

295
Q

PELVIC INFLAMMATORY DISEASE
What are the non-infective causes of PID?

A
  • Post-partum (retained tissue),
  • uterine instrumentation (hysteroscopy, IUCD),
  • descended from other organs (appendicitis)
296
Q

PELVIC INFLAMMATORY DISEASE
What are the non-STI infective causes of PID?

A

Gardnerella vaginalis,
H. influenzae,
E. coli.

297
Q

PELVIC INFLAMMATORY DISEASE
What is the clinical presentation of Fitz-Hugh-Curtis syndrome?

A

RUQ pain ± referred R shoulder pain if diaphragmatic irritation

298
Q

PELVIC INFLAMMATORY DISEASE
How is Fitz-Hugh-Curtis syndrome managed?

A
  • Inflammation + infection of liver (Glisson’s) capsule.
  • Leads to adhesions between liver + peritoneum, bacteria may spread from pelvis via peritoneal cavity, lymphatics or blood
  • RUQ pain ± referred R shoulder pain if diaphragmatic irritation
  • Laparoscopy to visualise + adhesiolysis
299
Q

GENITAL TRACT FISTULA
what is a genital tract fistula?

A

Abnormal connection between vagina and other organs, such as the bladder, colon, rectum

300
Q

GENITAL TRACT FISTULA
what are the causes of genital tract fistulas?

A

injury (primarily in childbirth),
surgery,
infection
radiation.

301
Q

GENITAL TRACT FISTULA
what are the different types?

A

➢ Vesicovaginal fistula
➢ Ureterovaginal fistula
➢ Urethrovaginal fistula
➢ Rectovaginal fistula
➢ Enterovaginal fistula
➢ Colovaginal fistula

302
Q

GENITAL TRACT FISTULA
what are the risk factors for genital tract fistulas?

A

➢ Childbirth
➢ Surgery
➢ Infection
➢ IBD
➢ Radiation

303
Q

GENITAL TRACT FISTULA
what are the symptoms of genital tract fistulas?

A

➢ Passage of gas, pus and fluid from the vagina
➢ Recurrent UTI’s
➢ Dyspareunia
➢ Irritation of vulva/vagina/anus/perineum

304
Q

GENITAL TRACT FISTULAS
what are the investigations for genital tract fistulas?

A

➢ Vaginal/anal examination (could use proctoscope or
speculum)
➢ Contrast tests (barium enema)
➢ Blue dye test ➔ put a tampon in the vagina then blue
dye in rectum. If tampon is stained = test positive
➢ CT, MRI, Ultrasound, Manometry

305
Q

GENITAL TRACT FISTULAS
what is the management for genital tract fistulas?

A

➢ Antibiotics, infliximab
➢ Surgery – must be done when there is no inflammation/infection
* Sewing of fistula
* Tissue graft
* Repairing anal sphincter
* Colostomy?
➢ Lifestyle changes → wash, avoid irritants, keep dry, loose clothes…

306
Q

OVERACTIVE BLADDER
what is an overactive bladder?

A

Involuntary leakage of urine accompanied by, or immediately preceded by, a strong desire
to pass urine (void).

Urgency, with or without urge urinary incontinence, usually with frequency and
nocturia is also defined as overactive bladder (OAB) syndrome →Detrusor overactivity.

307
Q

OVERACTIVE BLADDER
what are the causes of overactive bladder?

A

➢ Idiopathic
➢ Neurogenic DO in MS, Spina bifida, upper motor neuron lesions…
➢ Pelvic or incontinence surgery

308
Q

OVERACTIVE BLADDER
what are the risk factors for overactive bladder?

A

➢ Old age
➢ Pregnancy/childbirth
➢ Hysterectomy
➢ Obesity
➢ Family history

309
Q

OVERACTIVE BLADDER
what are the signs/symptoms of an overactive bladder?

A

➢ Symptoms of OAB include urinary frequency, urgency, urge incontinence, and nocturia.
➢ Provocative factors often trigger it, such as cold weather, opening the front door, or hearing
running water.
➢ Bladder contractions may also be provoked by increased intra-abdominal pressure (coughing
or sneezing), leading to complaint of stress incontinence, which may be misleading.
➢ Quality of life can be significantly impaired by the unpredictability and large volume of
leakage.

310
Q

OVERACTIVE BLADDER
what are the investigations for overactive bladder?

A

➢ Urine culture (Exclude UTI)
➢ Frequency/volume chart
➢ Urodynamics (looks for involuntary detrusor contractions during the filling phase in the
micturition cycle – spontaneous or provoked)

311
Q

OVERACTIVE BLADDER
how is it diagnosed?

A

➢ Urodynamic studies
➢ Exclusion of other factors → Metabolic diseases (hypercalcemia/diabetes), physical causes
(prolapse or fecal impactions), urinary pathology (UTI, cystitis) …

312
Q

OVERACTIVE BLADDER
what is the management for overactive bladder?

A
  1. Behavioral therapy (less liquids, avoid caffeine, avoid diuretics/antipsychotics)
  2. Bladder retraining
  3. Pharmacological interventions
    ➢ Anticholinergics (Oxybutynin): side effects include dry mouth, constipation, nausea,
    dyspepsia, palpitations, blurred vision…)
    ➢ Estrogens
    ➢ Botulinum toxin A
  4. Neuromodulation and nerve stimulation
  5. Surgical management – detrusor muscle myomectomy and augmentation cystoplasty…
313
Q

CERVICAL CANCER SCREENING
when is screening offered?

A

25-49yrs = every 3 years
50-64yrs = every 5 years
not offered to people over 64yrs

314
Q

CERVICAL CANCER SCREENING
when is cervical screening done in pregnancy?

A

it is usually delayed until 3 months post-partum unless missed screening or previous abnormal smears

315
Q

URINARY INCONTINENCE
what can cause stress incontinence?

A
  • low oestrogen in menopause
  • weakened pelvic floor
  • parity
  • pelvic surgery
316
Q

URINE INCONTINENCE
how does fistulas cause incontinence?

A
  • another outflow between urinary tract and vagina or bowel meaning urine can flow involuntarily
317
Q

URINARY INCONTINENCE
What is the purpose of cystogram with contrast?

A

visualise the bladder

318
Q

URINARY INCONTINENCE
What are some side effects of anti-muscarinics?

A
  • “Can’t see, spit, pee or shit” > caution in elderly as falls esp oxybutynin immediate release in frail
319
Q

URINARY INCONTINENCE
What is a caution of beta-3-adrenergic agonists?

A
  • C/I in uncontrolled HTN as stimulates SNS to increase BP, can lead to hypertensive crisis so monitor BP
320
Q

DYSMENORRHOEA
What is secondary dysmenorrhoea?

A

Secondary to endometriosis, adenomyosis, fibroids, PID, IUDs, cancer

MY REVISION - ALL PHASES (36 decks)

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