O&G Case 8, 15, 17, 18 Flashcards

1
Q

Whats the DDX for preterm labour?

A

● Preterm labour
● APH
pregnancy
● Placental abruption
● Uterine rupture

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2
Q

What is preterm birth and how common is it?

A

● Defined as “delivery before completion of 37+0 weeks gestation”
○ Later preterm: 34-37
○ Early preterm: <34
○ Very preterm: 28-<32
○ Extremely preterm: <28

● Apprxomimately 8% of births
● Threatened <3cm cervical dilation

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3
Q

What are the relative contributions of iatrogenic and spontaneous preterm birth?

A

● 2⁄3 spontaneous
○ Can have ROM without labour and can labour without ROM
○ Preterm prelabour rupture of membranes (PPROM)
● 1⁄3 iatrogenic preterm delivery for maternal or fetal indications
○ Preeclampsia
○ IUGR
○ Placenta praevia

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4
Q

Whatcan preterm birth cause in terms of morbidity (particularly neurodevelopmental) and perinatal mortality?

A

● Neurosensory issues
● Respiratory distress
○ Apnea of prematurity (cessation of breathing for >20s)
○ Transient tachypnoea of the newborn (TTN)
○ Bronchopulmonary dysplasia (BPD)
● Feeding intolerance and necrotising enterocolitis (NEC)
● Hypoglycaemia
● Hypothermia
● Jaundice at birth

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5
Q

What factors prior to pregnancy increase the risk of preterm birth?

A
  • Prev preterm and/or PPROM
  • Prev late miscarriage
  • Cervical incompetance / fibroids
  • Previous surgery i.e lETZ
  • Hx of termination <1cm, or C-section at full dilation
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6
Q

What factors during a pregnancy increase risk of preterm birth?

A
  • Maternal age <20 or >40
  • Low or high BMI
  • Polyhydraminos
  • Infection
  • Smoking
  • Placental abruption
  • ART
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7
Q

What are the common causes of preterm labour?

A

● Any stimulus for inflammation can precipitate preterm labour:
○ Infection
○ Bleeding
○ Uterine distension (due to multiple pregnancy or polyhydramnios)
● Premature activation of maternal or fetal hypothalamic-pituitary-adrenal axis
● Decidual haemorrhage

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8
Q

How can preterm labour be predicted?

A

● Risk scoring
● Cervical length (TVUS)
○ Shorter cervix → higher risk
● Vaginal biomarker swabs (mostly fFN)
○ Elevated fFN from 22-37 weeks gestation associated with higher risk of preterm labour

○ Can also use placental alpha macroglobulin-1 and phosphorylated insulin like growth factor binding protein 1 (Never heard of this in clincial practice)

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9
Q

How can preterm labour be prevented?

A

● Cervical cerclage
(between 12-14 weeks)
● Rescue cerclage
○ Already dilated cervix but no contractions yet
● Progesterone
○ For high risk woman
● Antibiotics
● Prophylactic tocolysis
○ Use to buy time for steroids to be taken and take effect or to transfer them to
appropriate centre for care
○ Nifedipine
○ Suppress premature labour
○ Calcium channel blocker
■ Stops influx of calcium which prevents uterine contractions

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10
Q

What must you give to a women with suspected preterm labour?

A

● Steroids
○ To prevent respiratory distress by accelerating pulmonary surfactant production
○ 11.4mg betamethasone x 2 24 hours apart
○ Give to women;
■ Increases risk of delivery <34+6 weeks gestation
■ When preterm birth is planned or expected within next 7 days (even within 24
hours)

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11
Q

What is the role of administering magnesium sulphate to women at preterm delivery?

A

● Magnesium sulphate
○ Usually in more preterm woman
○ Neuroprotection for infant
○ Reduces risk of cerebral palsy
○ Given as IV infusion over 4 hours just before birth

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12
Q

How would your management of a woman in preterm labour differ in a rural vs a tertiary hospital setting?

A

● Rural hospitals may not have NICU so need to factor in transfer of women to tertiary centre
● Tocolysis (nifedipine) will delay delivery by >48 hours to allow for transfer and administration
of antenatal corticosteroids and magnesium sulphate

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13
Q

What is the fetal fibronectin test and what is its role in assessing a woman in suspected preterm labour?

A

● fFN test detects the fFN (glue that attaches the fetal membranes to the decidua basalis) in the cervicovaginal fluid
● Elevated levels from 22-37 weeks associated with risk of preterm labour
● Strong negative predictive value → >99% of women with negative test will not delivery in next
10 days
● Do test before vaginal examination, ROM, or >48 hours from last sexual intercouse, if cervical
dilation <3cm → false positives (but can still be reassuring if negative)

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14
Q

What is tocolysis? What drug is commonly used for tocolysis in New Zealand?

A

● Tocolytics = medications used to suppress labour
● Nifedipine most common in NZ
○ Calcium channel blocker
■ Stops influx of calcium which prevents uterine contractions
○ Side effects
■ Transient palpitations
■ Headache
■ Flushing ○ Contraindications
■ Suspected or confirmed IU infection
■ Placental abruption
■ Significant hypotension
■ Maternal shock

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15
Q

What investigations might be useful when assessing a woman in suspected preterm labour?

A

● Blood test
○ FBC
○ CRP
○ G&h
● MSU
● High vaginal swab
● fFN (<34+6weeks)
● TVUS
○ Cervical length >30mm = negative
○ Cervical length <15mm = positive
● CTG (cardiotocography)
● Other vaginal biomarkers (PAMG-1)
● Ferning
○ Vaginal secretions mixed with amniotic fluid make a “fern-like” pattern under microscope
● Nitrazine test
○ Paper strips that detect pH changes in the vagina (amniotic fluid has higher pH than
vaginal fluid) ● USS
○ Fetal height and measurements
○ Liquor volume
○ Measurement of amniotic fluid volume to determine PPROM

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16
Q

What are the general principles of management for women in preterm labour?

A

Admit
- Confirm reg contractions
- FFN
- Cervical length and dilatation

Monitoring
● IV line → FBC, CRP, G&H, blood cultures if suspicious of infection
● Confirm fetal presentation by USS
● Continuous CTG (if in labour)

Give medicines

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17
Q

What medicines do you give for a preterm labour?

A

○ Administer corticosteroids
○ Magnesium sulphate (<30weeks)
○ Tocolysis (Nifidipine)
○ Prophylactic antibodies for threatened labour → UTI etc (to settle uterus down)
○ Prophylactic antibodies for group B (if in labour)

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18
Q

During labour what do you for a preterm?

A

Delayed cord clamping (if in labour)
● Prolongation of the time between the delivery of a newborn and the clamping of the umbilical
cord
● 60 seconds at birth
● Reduces neonatal mortality

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19
Q

How do you manage PPROM?

A

● Same management +
○ 10/7 oral erythromycin (reduce preterm birth)
○ Conservative management until >37 weeks gestation then IOL

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20
Q

How do you treat stress and urge incontinence?

A
  • Pelvic floor training
  • Estrogen cream
  • Bladder training
  • Surgical intervention
  • Duloxetine, Oxybutinin
  • Botox
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21
Q

What are the surgical interventions for incontinence?

A

○ Suspension/sling operations to elevate bladder neck and support urethra
○ Mid-urethral slings
■ Mesh tape is placed under the urethra through two to three small incisions in order to support the urethra
■ Increases sub-urethral support
○ Intramural urethral bulking agents
■ Bulking materials injected into the urethra and bladder neck which helps to close the lumen of the urethra
■ Increasing tissue mass increases outflow resistance
■ Evidence limited

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22
Q

What is prolapse?

A

Prolapse = muscles and tissues supporting pelvic organs become weak or loose Traditional terms describing pelvic organ prolapse

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23
Q

What is the new descriptive terms for prolapse?

A

● Anterior prolapse
○ Front wall of the vagina has herniated inward
○ Usually caused by the bladder or/and urethra shifting position and placing
pressure on the vaginal wall
○ This term includes the possibility of a cystocele, urethrocele and cystourethrocele.
● Posterior
○ Rectum to herniate into the vagina
○ Due to weakening of the musculature and connective tissue or damage to the
rectovaginal septum
○ This term includes the possibility of a rectocoele or enterocoele
● Apical
○ Tissue supporting the uterus weakens and the uterus slips downward, placing pressure on the vagina
○ Usually associated with trauma in childbirth
● Vaginal vault prolapse
○ Roof of the vagina collapses
○ Usually following hysterectomy
■ Will also have an enterocoele present

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24
Q

What are the symptoms and signs of prolapse?

A

● Feels like something is “coming down”
● Backache, urinary problems, dyspareunia
● Difficulty with micturition or defecation
● Discharge and bleeding (procidentia)
● Symptoms often less apparent in the morning

25
Q

How do you assess prolapse?

A

● Introitus inspected
● Woman asked to bear down (with the labia separated and the anus supported with a swab)
○ Vaginal wall prolapse will be evident ● Sim speculum exam in left lateral position
○ Examine vaginal walls and assess descent of cervix
● Bimanual exam
○ Assess uterine mobility and descent
○ Assess perineum and pelvic floor muscle tone
● If symptoms worse when standing → assess while standing
● May need neurological exam
○ Consider MS or neuropathy as cause for incontinence (urge)

26
Q

Whats the treatment for prolapse?

A

● Elicit from history (as it may impact management)
○ Menorrhagia?
○ Is family complete?
○ Normal sexual function?
● Address modifiable lifestyle factors that can contribute to the problem
● Consider and treat lack of estrogen (topical estrogen therapy)
● Physiotherapy for pelvic floor exercises
● Pessary (ring or cube)
● Surgery (repair +/- hysterectomy)
Pessaries

27
Q

Which investigations may be useful in assessing a patient with incontinence?

A
  • Urine dipstick
  • Serum creatinine
  • Bladder diary
  • Post void residual vol
  • Urodynamic testing
28
Q

What meds can exacerbate incontinence?

A
  • Diuretics
  • Alpha blockers,
  • Anti psychotics
  • Opioids
  • Sedatives
29
Q

What is the climacteric in the context of menopause?

A

Refers to the physical and emotional symtpoms of menopause

30
Q

What is menopause?

A

‘Menopause’ is referring to a specific event, the cessation of menses, and ‘climacteric’ to gradual changes of ovarian function that start before the menopause and continue thereafter for a while

31
Q

Describe the changes in the function of the hypothalamic-pituitary-ovarian axis which occur at menopause?

A

● Inhibin B levels begin to decline in perimenopause
○ Inhibin B is produced by granulosa cells in primary follicles (which are becoming
lower)
● Decreased ovarian feedback of inhibin (and estradiol) results in reduced negative feedback on pituitary for FSH release
● Higher plasma levels of FSH (increase 10-20x) stimulate a greater level of primordial follicles
and accelerates depletion of primordial reserve
○ LH also increases x 4-5
● Estrogen levels decrease by 80-90%
○ Oestradiol bigger reduction than oestrone
● Androgen decreases by 15%

32
Q

What symptoms are attributable to the physiological changes of the perimenopause?

A

Vasomotor changes → changes in level of estrogen and progesterone
● Hot flushes
● Night Sweats
● Palpitations
● Weakness
● Faintness
GU → due to reduction in estrogen
● Vaginal dryness
○ Atrophic changes
○ Reduction in vaginal lubrication
○ Rise in pH of vaginal fluids
Reduction in uterus size → due to reduction in estrogen Reduction of breast density → due to reduction in estrogen Osteoporosis → due to reduction in estrogen
Blood lipid changes
Behavioural and psychological changes → hormonal changes

33
Q

What tx or advice is given to women experiencing hot flushes, atrophic vaginal symptoms, prevention of osteoporosis?

A

● Hot flashes
- Avoid triggers
- Environmental temperature regulation
● Atrophic vaginal symptoms
- Vaginal estrogen creams
- Rings
- Tablet estrogen therapy
- Estrogen can reduce incidence of UTIs and features of overactive bladder
● Prevention of osteoporosis
- Smoking cessation
- Vitamin D
- Regular weight-bearing exercise

34
Q

What is the non-hormonal therapy for menopause?

A

● Selective estrogen receptor modulators
○ Tamoxifen
○ Ospemifene
○ Raloxifene
● Paroxetine (for vasomotor symptoms)
● Clonidine and/or gabapentin

35
Q

What are the types of HRT for menopause?

A

● Estrogen therapy (women without uterus)
● Estrogen + progestin (women with uterus)
○ Perimenopausal → cyclical
○ Postmenopausal → continous
● Oral or transdermal

36
Q

What are the risks associated with HRT in menopause?

A

○ Cancer
■ Unopposed estrogen therapy → endometrial cancer risk
■ Estrogen + progestin → breast cancer risk
○ CVD risk → DVT, PE, stroke
○ Gallbladder disease
○ Stress urinary incontinence

37
Q

What are the contraindications to HRT in menopause?

A

Cancer:
○ Undiagnosed vaginal bleeding
○ Breast cancer
○ Endometrial cancer
CVD:
○ Chronic liver disease
○ Hyperlipidaemia
○ Recent DVT/stroke
○ Coronary artery disease

pregnancy

38
Q

What are the important ddx for pevlic masses in children, adults of child baring and non-baring ages?

A

Urgent - childbearing age
● Ectopic (?rupture)
● Adnexal torsion
Urgent - non childbearing age(cancer)
● Primary malignancy in pelvic organs
● Metastases
Children (cysts)
● Physiological cysts as newborn
● Follicular ovarian cysts

39
Q

What are the potential other causes of pevlic masses in pre-menopausal women?

A

Hormonally driven
● Fibroid
● Endometrioma
● Physiological cyst
● Cysts
● PCOS

Non-hormonal
● Cysts adenoma
● Teratoma

Inflammatory
● Abscess
● Tubo Ovarian abscess
● Hydrosalpinx (often present with pain rather than mass)
○ Adhesions causing a backlog of fluid (expands fallopian tube)

40
Q

What are the post menopausal causes of pelvic masses?

A

Post-menopausal
● Same conditions as younger women
○ Hormonally driven things → present smaller
● Malignancy
● Metastatic disease

41
Q

Whats the trick for remembering different causes of pelvic masses?

A

Fetus
Flatus
Fibroids Flipping tumour
● Benign
○ Dermoid
○ Cystadenoma
○ Mucinous cystadenoma
○ Fibroma
● Malignant
○ Any organ
○ Leiomyosarcoma
○ Ovarian malignancy
■ Premenopausal
● Germ and stromal
■ Post-menopausal
● Epithelial
○ Serous
○ Mucinous

42
Q

What are the post menopausal tumor markers?

A

● CA 125 → serous cystadenoma, endometriosis, PID, pregnancy, pancreatitis
● Ca 19.9 → mucinous cystadenoma
● CEA

43
Q

What are the pre-menopausal tumor markers?

A

● AFP
● Beta HCG → germ cell tumours of ovary
● Lactate dehydrogenase
● CA 15-3 → breast cancer marker but also for benign ovarian masses

44
Q

What is the ‘risk of malignancy index’, and how is it useful in triage of women with ovarian masses?

A

RMI
● USS findings
● Clinical findings → such as ascites
● Menopausal status
● CEA marker finding

45
Q

What are the epidemiological features of and risk factors for ovarian cancer?

A

● Malignancy of older people ○ <55 years
● Genetic risk factors
○ BRCA1
○ BRAC2
○ HNPCC/lynch syndrome
● Hormonal
○ HRT
○ Nulliparity
○ Early menarche/late menopause
○ Infertility
○ Endometriosis
Arises from fallopian tubes → that’s why it is epithelial

46
Q

What are the main histological types of ovarian cancer?

A

● Epithelial
○ Serous
○ Mucinous
○ Endometrioid
● Germ cell

47
Q

What are the common presenting symptoms of ovarian cancer?

A

● In most cases, there are no early symptoms
● In advanced stages, the size and growth of the tumor can lead to:
○ Abdominal pain and ascites
○ Cancer cachexia
○ Possible disruption of menstrual cycle
○ Dyspnea due to malignant pleural effusion
○ Abdominal or pelvic mass
● Complication: tumor can cause ovarian torsion→ tissue infarction → surgical emergency
● The first symptom is often increasing abdominal girth (clothes no longer fit at the waist)

48
Q

How is ovarian cancer staged?

A

FIGO staging
Stage 1 → confined to ovaries Stage 2 → into pelvis
Stage 3 → into abdomen Stage 4 → distant mets

49
Q

What are the general principles of treatment for ovarian cancer?

A

Pelvic USS
CT chest/abdo/pelvis
If defined to ovary with no spread → surgical debulking
Most ovarian cancers present late and have spread → histology first (biopsy)
● Then chemotherapy first
● Stage 3 or less → chemo shrinks it down and can do interval debunking therapy
Krukenberg tumour
● Sister mary joseph nodule

50
Q

What are the common and important causes of postmenopausal bleeding?

A

Consider:
- Vulvovaginal atrophy
● Exogenous oestrogen
● Polyps
● Endometrial hyperplasia
● Endometrial cancer
● Cervical cancer

51
Q

What investigations may be indicated for a patient with postmenopausal bleeding?

A

○ FBC
○ Ferritin
● Smear and STI check
● Pelvic TVUSS
○ Endometrial thickness
■ <5mm unlikely to be endometrial cancer
■ Check ovaries, for polyps, fluid in endo cavity.
● Pipelle
○ Suctions/scrapes out some of endometrium
○ If 5mm-10mm on USS and get negative pipelle can discharge
○ If they have risk factors do a hysteroscopy anyway
● Hysteroscopy
○ Do straight away if >20mm
○ Directly visualises the endometrium with a microscope
○ Dilation and curettage
○ Outpatient or short GA

52
Q

What is the epidemiology of endometrial cancer?

A

● Most common gynae cancer in NZ and developed world
● Maori and pacific patients diagnosed at younger ages than NZ european
● Increasing → associated with high estrogen states (obesity is estrogen producing)
● Usually diagnosed early due to bleeding as common symptom
● Older demographic (<55 years) → mostly post-menopausal women

53
Q

What are risk factors for endometrial cancer?

A

● Age (mean age = 65)
● Unopposed estrogen therapy
○ PCOS
○ Tamoxifen (estrogen receptor modulator)
○ Anovulation
○ Nulliparity
○ Oestrogen only HRT
● Obesity (BMI >30)
● HTN
● Diabetes
● Previous endometrial polyps
● HNPCC
● Family history

54
Q

How does endometrial cancer typically present?

A

● Post-menopausal bleeding
● Intermenstrual bleeding (if perimenopausal)

55
Q

What are the general principles of treatment for endometrial cancer?

A

Treatment for endometrial cancer is surgical (unless otherwise contraindicated) with adjuvant
therapy (radiotherapy, chemotherapy, or hormonal therapy)

  • Check for spread (imaging)
  • Adjuvant use is determined by risk of recurrence
56
Q

How is endometrial cancer graded?

A

Type 1 = low grade oestrogen dependent/endometrioid = good prognosis ● Endometrioid adenocarcinomas = 80% of endometrial cancers
Type 2 = high grade oestrogen independent / non endometrioid cancers = poor prognosis

57
Q

How is endometrial cancer staged?

A

FIGO staging
● Stage 1: confined to uterus
● Stage 2: involves the cervix
● Stage 3: pelvic mets (spread to ovaries, fallopian tubes, vagina, or nearby lymph nodes)
● Stage 4: mets outside pelvis (bladder, rectum, abdomen)

58
Q

How is endometrial cancer treated?

A

(1) Low risk = Stage IA endometrial carcinoma without myometrial invasion => hysterectomy & BSO + post-operative observation + no adjuvant

(2) Stage IA endometrial carcinoma with myometrial invasion, 1B, or II => Intermediate risk => surgery + vaginal brachytherapy

● Stage IB and II higher risk so might offer EBRT

○ Brachytherapy = internal radiation treatment = radiation source placed close to the cancer through the vagina
● +/- chemotherapy (Paclitaxel and carboplatin)

High risk => stages III-IV and all non-endometrioid carcinomas => external beam radiotherapy + chemotherapy

59
Q

Write some notes on endometrial hyperplasia

A

● Hyperplasia divided into simple or complex (further divided into with or without atypia)
● Endometrial cancer may be preceded by, or co-exist with, premalignant hyperplasia =
complex endometrial hyperplasia with atypia
● Complex atypia = 80% risk of development of cancer ⇒ hysterectomy
● Simple <5% chance of developing into cancer
● Progesterone (high dose) treatment