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Phase 3A 2021 > Obstetrics and Gynaecology > Flashcards

Obstetrics and Gynaecology Flashcards

1
Q

Most common symptom of chalmydia?

A

Asymptomatic

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2
Q

Define stress incontinence

A

Involuntary leakage of urine on effort or exertion, or on sneezing/coughing

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3
Q

Risk factors for stress incontinence?

A

Increasing age
Past pregnancy and vaginal delivery
Post menopausal
Decreased oestrogen
High BMI
Constipation,
Hysterectomy,
Prolapse
family history, smoking, drugs eg ACEi

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4
Q

How to assess pelvic muscle tone?

A

Digitally
Use modified oxford grading system (0-5, rates strength of contraction)

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5
Q

What can you do initially to manage stress incontinence?

A

1) Lifestyle advice: decrease caffeine, advice on fluid intake, smoking cessation, weight loss if BMI over 30
2) 3 months pelvic floor training
3) surgery/duloxetine if surgery undesired by woman or contraindicated

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6
Q

What can be done in secondary care for stress incontinence?

A

Retro pubic mid-urethral sling
Autologous rectus fascial sling
Colposuspension
Intramural urethral bulking agents

Surgery is first line in secondary care. Can offer duloxetine as 2nd line

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7
Q

Describe an overactive bladder presentation

A

Urinary urgency associated with increased frequency and nocturia
Can be wet (incontinent) or dry (no incontinence)

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8
Q

Pathophysiology of overactive bladder?

A

Involuntary contractions of detrusor muscle during filling phase of micturition

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9
Q

Aetiology of overactive bladder?

A

Most=idiopathic
Can be associated with injury to pelvic/spinal nerves, surgery, MS, drugs eg diuretics/antidepressants/hrt

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10
Q

Mirabegron:

  • use
  • mechanism
  • contraindication
A
  • Overactive bladder if anticholinergics not suitable
  • relaxes sm and increases bladder capacity
  • uncontrolled bp
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11
Q

How to manage overactive bladder initially?

A

1) Lifestyle advice
2) Bladder training for at least 6 weeks
3) Anticholingergic e.g. oxybutynin/tolterodine/darifenacin
4) Mirabegron is another option

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12
Q

What are the side effects of anticholinergics?

A

Mad as a hatter - confused, COGNITIVE DECLINE
Hot as a beet - flushed skin
Hot as a dessert - high temp
Blind as a bat - dilated pupils
Dry as a bone - dry mouth+eyes, urinary retention, constipation

-anticholinergics are not suitable for patients with dementia

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13
Q

Secondary care options for overactive bladder?

A

Botulinum toxin type a injection into bladder wall
Percutaneous sacral nerve stimulation
Augmentation cystoplasty
Urinary diversion

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14
Q

Types of prolapse?

A
  • Cystocele
  • Uterovaginal
  • Rectocele
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15
Q

Pathophysiology of prolapse

A

Pelvic floor muscles and ligaments stretch and weaken over time and can no longer support the bladder/uterus/rectum so the organ slips down into and can protrude out of the vagina

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16
Q

Difference between cystocele and rectocele?

A

Cystocele=anterior vaginal prolapse (bladder falls through)
Rectocele=posterior vaginal prolapse (rectum falls through

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17
Q

Causes of prolapse/weakened pelvic floor muscles?

A

pregnancy

difficult labour

large baby

overweight

lower oestrogen after menopause

chronic constipation

chronic cough

repeated heavy lifting

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18
Q

Presentation of prolapse?

A

Asymptomatic

Heaviness/pulling in pelvis

Feeling like sitting on a small ball

Urinary sx, Bowel sx, Sexual sx

Tissue protruding from vagina

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19
Q

Is prolapse more common in pre or post menopausal women?

A

Postmenopausal women who have had at least one vaginal delivery

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20
Q

Management of prolapse?

A
  1. Lifestyle changes, pelvic floor exercises, oestrogen cream
  2. Pessaries
  3. Surgery: repair of tissues (sacroplexy, sacrospinous fixation) or hysterectomy
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21
Q

Types of female genital tract fistulae?

A

Vesicovaginal (bladder fistula, most common)
Uterovaginal
Urethrovaginal
Rectovaginal
Colovaginal
Enterovaginal (small intestine and vagina)

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22
Q

Why do fistulae develop?

A
  • injury
  • surgery
  • infection
  • radiation treatment
  • prolonged childbirth
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23
Q

What are potential problems with vesicovaginal or rectovaginal fistulae?

A
  • uncontrolled urinary or faecal incontinence
  • leakage out of the vagina
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24
Q

Treatment of genital tract fistulae?

A

Surgery

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25
Q

Describe a fibroid

A
  • Most common benign tumour in women
  • Smooth muscle cells and fibroblasts accumulate to form a hard, round, whorled tumour in the myometrium (uterine myoma)
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26
Q

When do you get fibroids and why?

A

During reproductive age as maintained by oestrogen and progestogen

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27
Q

Types of fibroid?

A
  • Submucosal (inner mucosal surface, extend into uterine cavity, cause significant menorrhagia, dysmenorrhoea and reduced fertility)
  • Intramural (don’t extend into uterine/peritoneal cavities, may cause menorrhagia and dysmenorrhoea)
  • Subserosal (outer serosal surface of uterus and extend into peritoneal cavity, commonly asx)

NB/ submucosal and subserosal may become pedunculated

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28
Q

Risk factors for fibroids?
What reduces risk?

A

RF: early menarche, late menopause, increasing age, obesity, Afro-carrib, family history,
Reduced risk: pregnancy and number of pregnancies

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29
Q

How does red degeneration of fibroids present?

A

Pregnant woman with a history of fibroids presenting with severe abdominal pain, vomiting, low-grade fever and tachycardia.

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30
Q

Presentation of fibroids?

A
  • Heavy menstrual bleeding (menorrhagia)
  • Prolonged menstruation, lasting more than 7 days
  • Abdominal pain, worse during menstruation
  • Bloating or feeling full in the abdomen
  • Urinary or bowel symptoms due to pelvic pressure or fullness
  • Deep dyspareunia (pain during intercourse)
  • Reduced fertility
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31
Q

Investigations for fibroids?

A

Hysteroscopy is the initial investigation for submucosal fibroids presenting with heavy menstrual bleeding.

Pelvic ultrasound is the investigation of choice for larger fibroids.

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32
Q

Management of fibroids?

A
  1. No management/safety netting
  2. If fibroid under 3cm: Mirena coil. Tranexamic acid 2nd line. Can also use COCP but contraindicated when surgery might be involved.
  3. Surgery +GnRH agonist: endometrial ablation, uterine artery embolisation, myomectomy or hysterectomy. GnRH agonists (e.g. goserelin acetate) used before surgery to reduce size of fibroid and make them less likely to bleed.
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33
Q

Complications of fibroids?

A
  • menorrhagia with iron deficiency anemia
  • compression of adjacent organs - urinary obstruction, constipation
  • infertility
  • torsion
  • red degeneration of fibroid (during 1st and 2nd trimester, fever, pain and vomiting)
  • miscarriage
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34
Q

Management of fibroids >3cm?

A

Medical:

  • Tranexamic acid/NSAIDS
  • Mirena coil – depending on the size and shape of the fibroids and uterus
  • Combined oral contraceptive - unless surgery seems likely
  • Cyclical oral progestogens

Surgical:

  • Uterine artery embolisation
  • Myomectomy
  • Hysterectomy
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35
Q

Medical management of fibroids less than 3cm?

A

For fibroids less than 3 cm, the medical management is the same as with heavy menstrual bleeding:

  1. Mirena coil
  2. Tranexamic acid/NSAIDS
  3. Combined oral contraceptive unless surgery is impending
  4. Cyclical oral progestogens

Surgical options if symptoms are severe:

  • Endometrial ablation
  • Resection of submucosal fibroids during hysteroscopy
  • Hysterectomy
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36
Q

Difference between uterine fibroid and polyp?

A

Fibroid = benign tumour of fibrous muscle tissue

Polyp = benign tumour of endometrial tissue

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37
Q

Types of ovarian cysts?

A
  • Functional cysts (most common - follicular cyst, corpus luteum cyst)
  • Cystadenomas (on surface of ovary)
  • Dermoid (teratomas- form from embryonic cells and can contain tissue eg hair/skin/teeth
  • Endometriomas
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38
Q

Complications of ovarian cysts?

A
  • Ovarian torsion - dermoid cysts and cystadenomas can grow large and move ovary
  • Rupture (severe pain and bleeding)
  • Necrosis
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39
Q

Investigations for ovarian cysts?

A

Pelvic exam
Pregnancy test (+=corpus luteum cyst?)
Pelvic USS
Laparoscopy
CA125 blood test (malignancy?)

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40
Q

Management of ovarian cysts?

A

Watchful waiting, oral contraceptives, surgery

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41
Q

What are functional cysts? What are the two types?

A

Cysts as a result of the menstrual cycle, when normal follicle continues to grow. Rarely painful, usually harmless and self limiting for 2-3 cycles
Follicular cyst and corpus luteum cyst (when follicle doesn’t rupture/release its egg or fluid accumulates inside follicle= corpus luteum grows into cyst)

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42
Q

Age distribution of ovarian torsion?

A

Bimodal :
15-30 and postmenopausal

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43
Q

Causes of ovarian torsion?

A 
Hypermobility of ovary 
Adnexal mass (most lesions=dermoid cysts or paraovarian cysts)

Younger= developmental abnormalities
Adults=ovarian tumours, polycystic ovaries, adhesions

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44
Q

Presentation of ovarian torsion?

A

Severe non specific lower abdo/pelvic pain (intermittent or sustained)
Nausea and vomiting
Adnexal tenderness
Commonly have increased WCC

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45
Q

Management of suspected ovarian torsion?

A

Urgent USS
Urgent surgery to prevent ovarian necrosis
Most ovaries non-salvageable: salpingo-oophorectomy
If non-infarcted= surgical untwisting

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46
Q

What is lichen sclerosus?

A
  • Chronic skin condition that presents with shiny, “porcelain-white” patches of skin.
  • Often affects genital and perianal areas.
  • Most common in women over 50
  • Thought to be autoimmune, linked to type 1 diabetes, thyroid, alopecia, vitiligo.
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47
Q

Presentation of lichen sclerosus?

A
  • Porcelain-white patches of skin
  • Skin tightness
  • Soreness and pain
  • Painful sex (superficial dyspareunia)
  • Erosions
  • Fissures
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48
Q

Complications of lichen sclerosus?

A
  • Infections (thrush, herpes, S. aureus)
  • Increased risk of squamous cell carcinoma (SCC)
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49
Q

Management of lichen sclerosus?

A
  1. Lifestyle measures: wash gently, non soap cleanser, loose clothing 2.
  2. Topical steroid ointment: clobetasol propionate 0.05%
  3. Other topical tx= oestrogen cream, tacrolimus ointment
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50
Q

What are tumour-suppressor genes?

A
  • Genes that act as ‘braking signals’ during G1 phase of the cell cycle, to stop or slow the cycle before S phase.
  • If they are mutated, cells grow uncontrollably = cancer
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51
Q

What are oncogenes?

A

Mutated genes whose presence can stimulate the development of cancer

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52
Q

Most common gynae cancer a)worldwide

b)in UK

A

a) Cervical
b) Endometrial

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53
Q

What are the types of cervical cancer?

A 
SCC (70-80%) 
Cervical adenocarcinoma (up to 10%)
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54
Q

What virus is associated with cervical cancer? Which subtypes specifically?

A 
Human papillomavirus (HPV) 
esp HPV16 and HPV18
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55
Q

What increases risk of HPV causing cervical cancer?

A
  • Missed vaccination
  • Early age intercourse
  • STI co-infection Immunocompromised
  • Smoking
  • OCP usage > 5yrs
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56
Q

What increases risk of contracting HPV?

A

Increased number of sexual partners, no condom use, age at first sexual intercourse

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57
Q

Presentation of cervical cancer?

A
  • Asx
    Intermenstrual/postcoital/postmenopausal bleeding
  • blood-stained vaginal discharge
  • mucoid/purulent discharge, pelvic pain/dyspareunia
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58
Q

What things are in place to help prevent cervical cancer?

A

HPV vaccination at age 12-13 for girls
Cervical cancer screening: every 3 years after 25

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59
Q

Describe the stages of cervical cancer?

A
  • Stage 1: Confined to the cervix
  • Stage 2: Invades the uterus or upper 2/3 of the vagina
  • Stage 3: Invades the pelvic wall or lower 1/3 of the vagina
  • Stage 4: Invades the bladder, rectum or beyond the pelvis
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60
Q

What is cervical intraepithelial neoplasia/CIN?

A
  • Grading system for the level of dysplasia (premalignant change) in the cells of the cervix.
  • CIN is diagnosed at colposcopy (not with cervical screening, thats diskaryosis - abnormal karyo/chromosomes/nucleus)
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61
Q

Management of cervical cancer?

A
  • Conservative
  • Stage 1: Hysterectomy/lymphadenectomy
  • Stage 2+: Radiotherapy, chemotherapy, palliative
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62
Q

What percentage of endometrial cancer cases are preventable?

a) 70.7%
b) 85.1%
c) 94.6%
d) 99.8%

A

d) 99.8%

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63
Q

Most common cancer in the UK?

A

Endometrial

9000 cases a year

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64
Q

Red flag symptom for endometrial cancer?

A

Postmenopausal bleeding

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65
Q

Presentation of endometrial cancer?

A
  • POST MENOPAUSAL BLEEDING
  • Postcoital bleeding
  • Intermenstrual bleeding
  • Unusually heavy menstrual bleeding
  • Abnormal vaginal discharge
  • Haematuria
  • Anaemia
  • Raised platelet count
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66
Q

RFs for endometrial cancer?

A
  • Unopposed oestrogen…
  • Postmenopausal
  • PCOS
  • Obese (oestrogen produced in fatty tissue)
  • Nulliparous
  • Oestrogen only HRT
  • on tamoxifen
  • High insulin (diabetes,PCOS)
  • Lynch syndrome
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67
Q

Protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Increased pregnancies
  • Cigarette smoking (anti-oestrogenic)
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68
Q

What type are most endometrial cancers?

A

Adenocarcinoma (90%)

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69
Q

How to investigate suspected endometrial cancer?

A
  • Transvaginal USS for endometrial thickness (normal is <4mm post-menopause)
  • Pipelle biopsy
  • Hysteroscopy with endometrial biopsy
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70
Q

Management of endometrial cancer?

A
  • hysterectomy +/- lymph nodes
  • radio/chemotherapy
  • progesterone therapy to slow progression
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71
Q

Presentation of ovarian cancer?

A
  • IBS like symptoms - constantly bloated, abdo distension, abdo discomfort, early satiety/loss of appetite
  • change in bowel habit
  • urinary frequency/urgency
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72
Q

RFs for ovarian cancer?

A
  • Age (peaks age 60)
  • BRCA1 and BRCA2 genes (consider the family history)
  • Increased number of ovulations - early onset periods, late menopause, no pregnancies, use of clomifene
  • Obesity
  • Smoking
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73
Q

What type are most ovarian cancers?

A

Epithelial

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74
Q

Investigations for suspected ovarian cancer?

Management?

A
  • CA125 blood test (>35 IU/mL is significant)
  • USS

Mx= surgery and chemo

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75
Q

Describe staging of ovarian cancer?

A 
i= ovary(ies)
ii= bowel/bladder into pelvis/womb
iii= into peritoneum, lymph
iv= distant organs
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76
Q

Presentation of vulval cancer?

A
  • RARE!
  • Over 65s
  • itch
  • pain
  • bleeding
  • lump
  • dysuria
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77
Q

Presentation of hydatidiform mole?

A

Dark brown-bright red vaginal bleeding during 1st trimester, severe N/V, sometimes passage of grape-like cysts, pelvic pressure or pain

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78
Q

RFs for vulval cancer?

A
  • Increasing age
  • VIN
  • lichen sclerosis
  • smoking
  • previous radiotherapy
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79
Q

What type of cancer is vulval cancer?

A

SCC - 90%

10% are adenocarcinomas

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80
Q

What is gestational trophoblastic disease?

A
  • A group of rare diseases in which abnormal trophoblast cells (tumours) grow inside the uterus after conception.
  • Premalignant: Hydatiform mole
  • Malignant: Invasive mole, choriocarcinoma
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81
Q

What is a hydatidiform mole? Two types

A

Molar pregnancy - abnormal growth (tumour) of trophoblasts

Complete= no formation of foetal tissue, placenta is abnormal and swollen 
Partial= maybe normal placental tissue, maybe formation of foetus (miscarried)
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82
Q

Pathophysiology of hydatidiform mole?

A
  • Complete mole: No fetal material - enucleated egg is fertilised by 2 sperms, only paternal DNA is expressed
  • Partial: May contain fetal material - egg is fertilised by 2 sperms
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83
Q

Complications of hydatidiform mole?

A

Molar tissue may remain and continue to grow= gestational trophoblastic neoplasia (GTN)
High level of HCG
May develop cancerous form= choriocarcinoma

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84
Q

Investigating hydatidiform mole?
Management?

A 
Ix= HCG, USS, histology, other bloods 
Mx= evacuation of uterus
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85
Q

What is endometriosis?

A
  • Endometrial tissue grows outside of the uterus - commonly involves ovaries, fallopian tube and pelvis lining
  • Tissue thickens, breaks down and bleeds but there is no way for the tissue to exit the body and so is trapped
  • Tissue becomes irritated, can form scar tissue and adhesions
  • If ovaries involved, cysts/endometriomas may form
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86
Q

What is Sampson’s theory of endometriosis?

A

Retrograde menstruation contributing to endometriosis

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87
Q

Presentation of endometriosis?

A
  • Chronic pelvic pain often associated with periods
  • Dysmenorrhoea
  • Deep dyspareunia
  • Pain on bowel movements or urination
  • Excessive bleeding
  • Infertility
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88
Q

How to diagnose endometriosis?

A

Pelvic exam, USS, MRI can point towards diagnose
Only way to formally diagnose= laparoscopy

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89
Q

How to manage endometriosis?

A
  • Simple analgesia= NSAIDs and tranexamic acid
  • Ovulation suppression (tricyclic COCP, Mirena coil, GnRH analogues)
  • Laser/diathermy ablation
  • Radical hysterectomy and oophorectomy
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90
Q

What increases marker CA125?

A

Ovarian cancer
Also: adenomyosis, ascites, endometriosis, menstruation, breast cancer, ovarian torsion, endometrial cancer, liver disease, metastatic lung cancer

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91
Q

What is found in the functional layer of the endometrium?

A

Endometrial glands! Endometrium is glandular tissue that secretes glycogen etc. in secretory phase, in preparation for implantation of fertilised egg.

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92
Q

What is adenomyosis?

A

Uterine condition of ectopic endometrial tissue (adeno) in the myometrium

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93
Q

RFs for adenomyosis?

A

High oestrogen exposure eg short menstrual cycles and early menarche, or treated with tamoxifen

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94
Q

Presentation of adenomyosis?

A
  • Asx
  • multiparous women of reproductive age
  • Potential sxs= dysmenorrhoea, menorrhagia, dyspareunia, chronic pelvic pain
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95
Q

What are the 3 types of adenomyosis?

A

Diffuse, focal, cystic

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96
Q

Investigations for adenomyosis?

A
  1. Transvaginal ultrasound
  2. Transabdominal ultrasound, MRI
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97
Q

Management of adenomyosis?

A

If contraception not wanted:

  • Tranexamic acid when there is no associated pain (antifibrinolytic – reduces bleeding)
  • Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)

If contraception is wanted or acceptable, same as endometriosis:

  1. Mirena coil (first line)
  2. Combined oral contraceptive pill
  3. Cyclical oral progestogens
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98
Q

Define dysfunctional endometrial bleeding?

A

Abnormal uterine bleeding in absence of recognisable pelvic pathology, general medical disease or pregnancy

Mainly caused by imbalance in sex hormones
Abnormal may= intermenstrual, heavy, clots, bleeding>7 days, short or long cycles, spotting

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99
Q

When do you see lots of dysfunctional endometrial bleeding?

A

Early on in puberty

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100
Q

how to manage dysfunctional endometrial bleeding?

A
  • Oral contraceptives
  • Hormonal contraceptives.
  • Mostly a temporary condition- manage any anaemia
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101
Q

How is androgen insensitivity syndrome inherited?

A

X linked recessive

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102
Q

How does androgen insensitivity syndrome present?

A

Complete or partial, partial has more ambiguous px eg micropenis or clitoromegaly/hypospadias etc
External female phenotype, genotype is male
Undescended testes, female external genitalia, absence of internal female genitalia, breast tissue, lack of pubic hair/facial hair, taller than female average
Infertile and increased risk of testicular cancer

Primary amenorrhoea

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103
Q

What can be seen in the bloods of someone with androgen insensitivity syndrome?

A

Increased LH
Normal/raised FSH
Increased oestrogen
Normal/raised testosterone

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104
Q

How to manage androgen insensitivity syndrome?

A

Bilateral orchidectomy, oestrogen therapy, vaginal dilators/surgery to create adequate vaginal length
Raised as girls/women generally

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105
Q

Incidence of premature menopause

A

1 in 100 (occurring in under 40s)

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106
Q

Common menopause symptoms?

A

Hot flushes, night sweats, vaginal dryness, difficulty sleeping, low mood or anxiety, reduced libido, memory and concentration problems

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107
Q

What gonadotrophin is higher in menopause?

A

FSH

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108
Q

how to manage menopause?

A

HRT, simple measures for sweats/flushes, CBT, antidepressants, testosterone gel (libido), vaginal oestrogen, calcium/vit d/bisphosphonates (osteoporosis risk)

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109
Q

What is atrophic vaginitis?
When does it occur?

A

Thinning, drying and inflammation of vaginal walls due to decreased oestrogen

Occurs: perimenopause, menopause, surgical menopause, during breast feeding, contraceptive pills, pelvic radiation, chemo, breast cancer hormonal treatment

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110
Q

Describe GSM (genitourinary syndrome of menopause)

A

Dryness, burning, discharge, itching, burning/urinary/frequency, recurrent UTIs, incontinence, postcoital bleeding, dyspareunia, decreased vaginal lubrication during intercourse, shortening and tightening of vagina

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111
Q

Management of atrophic vaginitis?

A

Vaginal moisturisers, water-based lubricant, topical oestrogen, vaginal dilators, topical lidocaine, regular intercourse

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112
Q

Precocious and late menarche?

A

Precocious=under 9
Late= over 15 years

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113
Q

Describe physiology of menarche

A

Pulsatile GnRH from hypothalamus stimulates pituitary production of FSH and LH. This increases ovarian production of oestrogens (oestradiol and androgens).
Oestradiol causes maturation of ovarian follicles
Increased oestrogen causes uterine endometrial proliferation and eventually an LH surge, causing ovulation or rupture of dominant ovarian follicle
Progesterone (adrenal cortex and ovaries) causes thickening of endometrium

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114
Q

Presentation of endometrial polyps?

A

Irregular menstrual bleeding, intermenstrual bleeding, menorrhagia, bleeding after menopause, infertility

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115
Q

RFs for endometrial polyps?

A

Oestrogen dependent: peri/postmenopausal, hypertension, obesity, tamoxifen

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116
Q

How to investigate and manage endometrial polyps?

A

Ix: transvaginal USS, hysteroscopy, endometrial biopsy
Mx: watchful waiting, short term meds (progestins and GnRH agonists), surgical removal

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117
Q

Most common location for ectopic pregnancy?

A

Fallopian tube (tubal pregnancy)

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118
Q

RFs for ectopic pregnancy?

A

Previous ectopic pregnancy, inflammation or infection (STIs), fertility treatments, tubal surgery, birth control (IUD and tubal ligation/tubes tied), smoking

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119
Q

Presentation of ectopic pregnancy?

A

Positive pregnancy test, early presentation pregnancy (missed period, breast tenderness, nausea), light vaginal bleeding and pelvic pain
NB/ if blood leaks from fallopian tube may feel shoulder pain or urge to have bowel movement
Rupture if continued growth- shock and life threatening

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120
Q

How to manage an ectopic pregnancy?

A

Methotrexate injection for early ectopic without unstabke bleeding
Laparoscopy- salpingostomy/salpingectomy (ectopic/ectopic and tube removed)
Emergency surgery

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121
Q

Incidence of polycystic ovaries and polycystic ovary syndrom?

A

Polycystic ovaries= up to 33% of women of reproductive age
PCOS= 5-15% of women of reproductive age

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122
Q

Pathophysiology of PCOS?

A 
Excess androgens (ovary theca cells- due to hyperinsulinaemia or increased LH) and insulin resistance \> hyperinsulinaemia 
\> increased androgens and decreased SHBG (sex hormone binding globulin) in liver, increased LH due to increased production (anterior pituitary) and increased oestrogen in some women (causing hyperplastic endometrium)
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123
Q

Presentation of PCOS?

A

Peripubertal -mid 20s
Oligomenorrhoea (under 9 periods/year), infertility/subfertility, acne and hirsutism, alopecia, obesity/difficulty losing weight, psych symptoms, sleep apnoea, may have acanthosis nigricans

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124
Q

Criteria for PCOS? describe

A

Rotterdam criteria- need at least 2:

Polycystic ovaries, oligo-ovulation/anovulation, clinical and/or biochemical signs of hyperandrogenism

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125
Q

Investigating PCOS?

A

Testosterone (normal or high), SHBG (normal or low), LH (high), USS, fasting glucose/oral glucose tolerance test

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126
Q

Management of PCOS?

A

MDT management, advise on cardiac risks
Weight control and exercise, COC pills or IUS, metformin can be used

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127
Q

Complications of PCOS?

A

Infertility, endometrial hyperplasia/cancer, CVD, T2DM, sleep apnoea

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128
Q

Abnormal formations of uterus ?

A

Due to incomplete fusion of mullerian or paramesonephric ducts:
Complete failure (double vagina, cervix and uterus)
Some fusion (single vagina and cervix, double single horned uteruses partially fused)
Septate uterus (midline septum)
Arcuate
Unicornuate

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129
Q

Abnormal formations of vagina?

A

Vaginal agenesis, vaginal atresia, mullerian aplasia, transverse vaginal septa

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130
Q

Turner syndrome genotype?

A

45X

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131
Q

What is Asherman syndrome?
How to manage?

A

Formation of intrauterine adhesions; usually due to injury to endometrium
Tendency to develop them after pregnancy

Mx; lysis of adhesions via hysteroscopy

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132
Q

Presentation of asherman syndrome?

A

Infertility, loss of pregnancy, menstrual abnormalities, abdominal pain

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133
Q

How might prolactinoma present?

A

Galactorrhoea, amenorrhoea/oligomenorrhoea, anovulatory cycles, infertility, hirsutism, decreased libido

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134
Q

How to manage prolactinoma?

A

Dopamine agonists eg cabergoline
Surgery
Oestrogen contraception

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135
Q

What can cause pelvic inflammatory disease?

A

STIs esp gonorrhoea and chlamydia
Mycoplasmas, flora, strep, TB

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136
Q

Presentation of pelvic inflammatory disease?

A

Bilateral lower abdominal pain, deep dyspareunia, abnormal bleeding, purulent discharge, may have fever, may have N/V, urinary symptoms, proctitis and adnexal mass

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137
Q

Investigating PID?

A

STI swabs, pregnancy test, laparoscopy (single best diagnostic test), exclusions eg UTI

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138
Q

How to manage PID?

A

Analgesia
Abx immediately before swab results- IM ceftriaxone 500mg stat then doxycyline 100mg bd and metronidazole 400mg bd for 14 days
Partner notification and treatment

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139
Q

Recent coil insertion but got PID?

A

If coil recently inserted can leave in, but if no response to abx in 48-72 hour, remove and prescribe any emergency contraceptives if needed

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140
Q

Complications of PID?

A

Infertility, ectopic pregnancy, chronic pelvic pain, perihepatitis, tubo-ovarian abscess, reactive arthritis, preterm delivery, vertical transmission

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141
Q

How many stages of labour are there?

A

3

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142
Q

describe the 1st stage of labour

A

Cervix dilation.
Early labour:
-Latent phase- cervix starts to soften, irregular contractions=hours-days
-Established labour- cervix dilated to 4cm and regular contractions
-Established labour- dilation 6-10cm

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143
Q

How can you speed up labour?

A

ARM=artificial rupture of the membranes
or oxytocin drip

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144
Q

Describe the 2nd stage of labour

A

Full cervix dilation up to birth aka the pushing stage

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145
Q

How long does 2nd stage of labour generally take in primiparous women? Multiparous women?

A 
Primi= less than 3 hours 
Multi= less than 2 hours
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146
Q

Describe the 3rd stage of labour

A

Delivery of placenta

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147
Q

Two ways of 3rd stage of labour happening?

A

Active=oxytocin IM injection
or
Physiological= natural where the cord isn’t cut until it’s stopped pulsing, can take about an hour

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148
Q

Pros and cons of active 3rd stage of labour?

A 
Pros= much faster delivery of placenta and lowers risk of postpartum haemorrhage 
Cons= increased risk of nausea and can make afterpains worse
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149
Q

What counts as premature labour?

A

Regular contractions resulting in dilation of cervix after week 20 and before week 37 of pregnancy

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150
Q

Presentation of premature labour?

A

Contractions, constant low dull back ache, pelvic pressure, mild cramps, spotting or light bleeding, rupture of membranes, change in vaginal discharge

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151
Q

Potential risk factors for premature labour?

A

Multiple pregnancy, previous preterms, shortened cervix, cigarettes, drugs, infections, chronic conditions, stress, polyhydramnios, foetal birth defect, age of mother

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152
Q

How to try to prevent premature labour?

A

Regular prenatal care, healthy diet, avoid risky substances, pregnancy spacing, cautious with IVF/how many embryos

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153
Q

How should you manage premature labour?

A

If unwell, speed up delivery with oxytocin/induction/C-section
If over 34 weeks, then let labour progress naturally
Corticosteroids if between 23 and 34 weeks if risk of delivery in next week
Tocolytics can be used for around 48 hours to buy time for course of steroids/transfer time
Magnesium sulfate venous infusion to reduce risk of cerebral palsy for under 34 weeks

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154
Q

What to give if in labour before 34 weeks gestation?

A

Magnesium sulfate, steroids
Tocolytics if need to buy time (about 48 hours)

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155
Q

Define premature rupture of membranes (prom)?

A

Rupture of foetal membranes at least one hour prior to the onset of labour in over 37 weeks gestation pregnancies

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156
Q

How common is premature rupture of membranes?

A

10-15% term pregnancies

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157
Q

Define preterm premature rupture of membranes (p-prom)

A

rupture of membranes at least one hour prior to onset of labour in under 37 weeks of gestation pregnancies

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158
Q

Incidence of preterm premature rupture of membranes

A

Associated with 40% preterm deliveries

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159
Q

What comprises foetal membranes?

A

chorion and amnion

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160
Q

What can cause premature rupture of membranes?

A

Early activation of normal physiological processes (enzymes)
Infection (inflammatory markers weaken the membranes)
Genetic predisposition

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161
Q

Risk factors for premature rupture of membranes?

A

Smoking, previous PROM, vaginal bleeding, lower genital tract infection, invasive procedures eg amniocentesis, polyhydramnios, multiple pregnancy, cervical insufficiency

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162
Q

Presentation of premature rupture of membranes?

A

“broken waters”- painless popping sensation then gush of watery fluid or non specific eg gradual leakage

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163
Q

Management of suspected premature rupture of membranes?

A

Speculum exam- pooling in posterior vaginal fornix (need to lie down for at least 30 mins to see this)
Avoid digital vaginal examination until active labour
High vaginal swab- if GBS then start clindamycin/penicillin during labour

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164
Q

Complications of premature rupture of membranes?

A

Chorioamnionitis, oligohydramnios, neonatal death, placental abruption, umbilical cord prolapse

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165
Q

Commonest associations with placental insufficiency and low birthweight?

A

DM, htn, clotting disorders, anaemia, medications especially blood thinners, smoking, drug abuse especially cocaine/heroin/methamphetamine, placental poor attachment or placental abruption

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166
Q

Risk of placental insufficiency

  • to mum?
  • to baby?
A 
Mum= preeclampsia, placental abruption, preterm labour and delivery 
Baby= greater risk of o2 deprivation, hypothermia, hypoglycaemia, hypocalcaemia, polycythaemia, premature, c-section, stillbirth, death
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167
Q

What is a miscarriage?
2 types?

A

Loss of pregnancy before 24 weeks gestation
Early miscarriage= more common- 1st trimester (before 12-13 weeks)
Late miscarriage=13-24 weeks

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168
Q

How common is miscarriage?

A

Very! 20-25% of pregnancies

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169
Q

Risk factors for miscarriage?

A

Over 30, previous miscarriage, obesity, chromosomal abnormalities, smoking, uterine anomalies, previous uterine surgery, anti-phospholipid syndrome, coagulopathies

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170
Q

Presentation of suspected miscarriage?

A

Vaginal bleeding, cramping pain, incidental finding on USS
Positive pregnancy test and bleeding +/- pain

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171
Q

Investigations for suspected miscarrage?

A

Transvaginal USS is 1st line
Serum b-HCG if us not available

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172
Q

Management of miscarriage?

A

If late miscarriage- need anti- D prophylaxis if rh neg
Conservative/expectant=allow to pass naturally
Medical=vaginal misoprostol (prostaglandin analogue- stimulates cervical ripening and contractions)
Surgery= manual vacuum aspiration if early miscarriage or for evacuation of retained products of conception

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173
Q

Classification of miscarriages?

A

Threatened, inevitable, missed, incomplete, complete, septic

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174
Q

Describe a threatened miscarriage

A

Mild bleeding +/- pain, cervix close - still a viable pregnancy

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175
Q

Describe an inevitable miscarriage

A

Heavy bleeding, clots, pain, cervix open- internal cervical os opened
Foetus viable or non viable

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176
Q

Describe a missed miscarriage

A

Asx or hx of threatened miscarriage, ongoing discharge, small for dates uterus

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177
Q

Describe an incomplete miscarriage

A

Products of conception partially expelled, sxs of missed miscarriage or bleeding/clots

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178
Q

Describe a septic miscarriage

A

Infected POC: fever, rigors, uterine tenderness, bleeding/discharge, pain

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179
Q

Define recurrent miscarriage

A

At least 3 consecutive pregnancies with miscarriage

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180
Q

What is gestational diabetes?

A

Any degree of glucose intolerance with onset of first recognition during pregnancy

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181
Q

Why does gestational diabetes occur?

A

Progressive insulin resistance in pregnancy and insulin requirements rise by 30% during pregnancy
A borderline pancreatic reserve is unable to respond to higher requirements and causes transient hyperglycaemia (insulin resistance falls after pregnancy)

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182
Q

RFs for gestational diabetes?

A

BMI over 30, asian, previous gestational dm, 1st degree relative with dm, PCOS, previous macrosomic baby (pver 4.5kg)

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183
Q

How would gestational diabetes present? What investigation

A

Px= asx or DM sxs eg polyuria/dipsia and fatigue
Ix=OGTT

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184
Q

How to manage gestational diabetes?

A

Lifestyle advice, capillary glucose measurements qds, may need metformin (glibenclamide 2nd line) or insulin
Deliver at 37-38 weeks if on treatment
Stop treatment immediately after delivery then 6-13 weeks later do a fasting glucose test to confirm transience

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185
Q

Foetal complications of gestational diabetes

A

Macrosomia, organomegaly, erythropoiesis, polyhydramnios, increased rate of pre-term delivery
Neonatal hypoglycaemia

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186
Q

Pathophysiology of pre-eclampsia

A

Incomplete remodelling of spiral arteries causes a high resistance low flow uteroplacental circulation (the constrictive muscular walls are maintained)
Increased BP, hypoxia and oxidative stress leads to inadequate uteroplacental perfusion causing a systemic inflammatory response and endothelial cell dysfunction

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187
Q

Risk factors for pre-eclampsia? 3 moderate and 3 high

A 
Moderate= nuliparity, over 39 years, BMI at least 35, FH, pregnancy interval over 10 years, multiple pregnancy 
High= chronic htn, htn/pre-eclampsia/eclampsia in previous pregnancy, CKD, DM, autoimmune diseases
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188
Q

How to do and who to consider prophylaxis for pre-eclampsia?

A

75mg aspirin/day from 12 weeks to birth
In women with at least 1 high or at least 2 moderate risk factors

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189
Q

Pre-eclampsia potential features

A

hypertension (2 occasions at least 4 hours apart, over 140/90)
significant proteinuria
over 20 weeks gestation

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190
Q

How does pre-eclampsia present?

A

Asx, frontal headaches, visual disturbance, epigastric pain, hyperreflexia, sudden onset non-dependent oedema

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191
Q

Classification of pre-eclampsia

A

Mild= 140/90-149/99
Mod=150/100-159/109
Severe= at least 160/110 and proteinuria or at least 140/90+sxs+proteinuria

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192
Q

Does pre-eclampsia resolve?

A

Yes, following placental delivery

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193
Q

Management of pre-eclampsia?

A

Monitoring, VTE prevention, antihypertensives= labetalol (1st line), also nifedipine/methyldopa, delivery!
After delivery, monitor BP for 2 days then once every 3-5 days

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194
Q

Maternal complications of pre-eclampsia?

A

HELLP syndrome (haemolysis, elevated liver enzymes, low plateletes), eclampsia, aki, dic, ards, htn, stroke, death

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195
Q

What is eclampsia?

A

Pre-eclampsia and convulsions
Obstetric emergency

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196
Q

Presentation of eclampsia?

A

Most seizures occur in postnatal period
New onset tonic clonic type seizure, lasting about 60-75 seconds with variable post ictal period
S+Ss relating to end organ dysfunction

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197
Q

Foetal complications of eclampsia?

A

Intrauterine growth restriction, prematurity, IRDS, foetal death, placental abruption

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198
Q

How to manage eclampsia?

A

Resuscitation
Seizure cessation with magnesium sulfate
BP control with labetalol and hydralazine
Prompt delivery via C section after mother stabilised
Postpartum and postnatal monitoring and follow up

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199
Q

Why might people with essential hypertension prior to pregnancy not need treatment during their pregnancy?

A

Physiological drop in BP during pregnancy, so may even get hypotension, or sustain BP below 110/70

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200
Q

What is target BP during pregnancy?

A

Less than 135/85

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201
Q

How to manage essential hypertension during pregnancy?

A

Stop ACEi/ARB and start labetalol (1st line)
Nifedipine (2nd line), methyldopa (3rd line)
From 12 weeks onwards 75-150mg aspirin daily

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202
Q

Causes of antenatal haemorrhage?

A

Placental abruption, placenta praevia, vasa praevia, uterine rupture, local genital causes

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203
Q

Management of APH?

A
  • corticosteroids 24+0-36+6 weeks
  • active management of third stage of labour
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204
Q

Should women with APH be hospitalised?

A

Women presenting with spotting who are no longer bleeding and where placenta praevia has been excluded can go home.
All women with APH heavier than spotting and women with ongoing bleeding should remain in hospital at least until the bleeding has stopped.

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205
Q

Complications of APH?

A

Maternal: Anaemia, infection, shock, consumptive coagulopathy, PPH

Fetal: Hypoxia, SGA and FGR, prematurity, fetal death

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206
Q

What is placenta praevia? 2 types?

A

Placenta fully or partially attached to lower uterine segment
Minor= low placenta, but doesn’t cover internal cervical os
Major= placenta lies over internal cervical os

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207
Q

RFs for placenta praevia?

A

Previous C-section (higher risk with greater number), high parity, age over 40, multiple pregnancy, PMH, endometritis

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208
Q

What examination should you NOT perform in suspected placenta praevia?

A

Digital vaginal exam

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209
Q

How does placenta praevia present?

A

Painless vaginal bleeding

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210
Q

How to manage placenta praevia?

A

ABCDE
If incidental finding at 20 week scan; minor= repeat scan at 36 weeks, major=repeat scan at 32 weeks
C-section=safest mode of delivery (38 weeks for major)
Anti-D within 72 hours of onset of bleeding to Rh neg mother

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211
Q

What is placenta accreta?

A

Placenta grows too deeply into uterine wall and part/all of placenta remains attached after childbirth- can cause severe haemorrhage

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212
Q

3 degrees of placenta accreta?

A

Accreta - placenta ATTACHES to the surface of the myometrium

Increta - placenta INVADES deeply into the myometrium

Percreta - placenta PERMEATES past the myometrium and perimetrium, potentially reaching other organs

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213
Q

RFs for placenta accreta?

A

PMH
Previous C section and other uterine surgery e.g. endometrial curretage due to miscarriage/abortion
Low-lying placenta or placenta previa
Maternal age, multigravida

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214
Q

Management of placenta accreta?

A

Confirm on MRI
C-section and hysterectomy (helps to prevent haemorrhage if there’s an attempt to separate placenta)
Deliver between 34-36+6 if complicated, 36-37 weeks if uncomplicated

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215
Q

What is placenta increta?

A

Placenta invades into muscles of uterus (form of placenta accreta)

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216
Q

What is placental abruption? Why does it occur?

A

Part/all of placenta separates from uterine wall prematurely (cause of antenatal haemorrhage)
Due to rupture of maternal vessels within basal layer of endometrium- blood accumulates and splits the placental attachment

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217
Q

2 types of placental abruption?

A

Revealed- blood drains through the cervix
Concealed- bleeding remains within uterus causing a retroplacental clot

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218
Q

RFs for placental abruption?

A

PMH (most predictive factor), pre-eclampsia/htn, abnormal lie of baby, polyhydramnios, abdo trauma, smoking, drugs, bleeding in 1st trimester, thrombophilia, multiple pregnancy

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219
Q

Presentation of placental abruption?

A

Painful bleeding

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220
Q

Management of placental abruption?

A

ABCDE
Emergency delivery due to maternal and/or foetal compromise
Induction of labour
Conservative
Anti-D if applicable within 72 hours of bleeding onset

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221
Q

How to reduce the risk of a retained placenta?

A

Use active management in third stage of labour with syntocinon

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222
Q

Presentation of retained placenta?

A

Fever, badly smelling discharge, heavy bleeding, pain

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223
Q

Management of retained placenta?

A

Empty bladder/change position
Pull on umbilical cord
Surgery to scrape it away

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224
Q

What is uterine rupture? Two types

A

Obstetric emergency: Full thickness disruption of uterine muscle and overlying serosa, typically during labour, can extend to affect bladder or broad ligament
Incomplete= intact peritoneum over uterus, uterine contents remain in uterus
Complete= torn peritoneum, uterine contents can escape into peritoneal cavity

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225
Q

RFs for uterine rupture?

A

Previous C-section/uterine surgery, induction, obstruction of labour, multiple pregnancy, multiparity

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226
Q

Presentation of uterine rupture?

A

Non specific
Sudden, severe abdo pain persisting between contractions, may have vaginal bleeding

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227
Q

Management of uterine rupture?

A

ABCDE
Emergency C section and uterus repair or hysterectomy
(decision-incision interval should be less than 30 mins)

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228
Q

What is cervical show?

A

Small amount of bleeding from vagina caused by rupture of small blood vessels in cervix due to contractions- slow cervical dilatation
Part of labour

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229
Q

What is vasa praevia?

A

Foetal blood vessels run near/over internal cervical os- likely to rupture in active labour as unprotected by placental tissue or wharton’s jelly of umbilical cord

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230
Q

How does vasa praevia present? (classic triad)

A

rupture of membranes
painless vaginal bleeding
fetal bradycardia

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231
Q

How to manage vasa praevia?

A

Emergency C sections
Improved mortality rates if picked up on USS and using a planned C section

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232
Q

What differentiates antepartum haemorrhage from miscarriage?

A

Timing
Miscarriage= before 24 weeks
Antepartum haemorrhage= bleeding from birth canal after 24th week of pregnancy until second stage of labour complete

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233
Q

Causes of antepartum haemorrhage?

A

Major ones= placenta praevia and placental abruption
Also= local causes (infection, trauma, tumours), vasa praevia, uterine rupture, inherited bleeding problems

234
Q

How to differentiate placenta praevia from placental abruption clinically?

A

Both=bleeding
Pain=abruption
Painless=praevia

235
Q

What volume of blood for minor antepartum haemorrhage?

A

Blood loss less than 50ml and stopped

236
Q

What constitutes major anterpartum haemorrhage?

A

50-1000ml blood loss with no signs of shocks

237
Q

What constitutes massive antepartum haemorrhage?

A

Over 1000ml blood loss and/or signs of shock

238
Q

Management of antepartum haemorrhage?

A

ABCDE
DO NOT attempt vaginal examination
Consider delivery
Urgent USS, foetal monitoring (CTG), anti-D if indicated

239
Q

Minor and major primary post partum haemorrhages?

A 
Minor= 500-1000ml within 24 hours 
Major= over 1000ml within 24 hours delivery or signs of shock
240
Q

Two broad groups of causes of post partum haemorrhage?

A

Primary and secondary

241
Q

Primary causes of post partum haemorrhage?

A

Four Ts= tone (uterine atony, distended bladder), trauma, tissue (retained placenta or clots), thrombin (coagulopathy)
Most common=uterine atony then retained placenta

242
Q

Secondary causes of post partum haemorrhage?

A

infection (endometritis) or retained products of conception, subinvolution of placental implantation site, pseudoaneurysms, AV malformation

243
Q

How to manage post partum haemorrhage?

A

Resuscitation
2 14/16 G cannulas
Crystalloid infusion for minor
Blood transfusion for major
Catheterise
Cross match or O neg
If uterine atony is cause- fundal rub, bimanual uterine compression to stimulate contraction, oxytocin, ergometrine, carboprost, misoprostol
If medical management not working then surgery
Antibiotics for endometritis

244
Q

What is sheehan’s syndrome?

A

In women who lose life threatening amount of blood in childbirth or have severely low BP, causes hypoxia which causes pituitary gland damage and subsequent HYPOPITUITARISM

245
Q

How does sheehan’s syndrome present?

A

Presents slowly over months/years, but may also have inability to breastfeed
S+Ss: a/oligomenorrhoea, slowed mental function, weight gain, hypothyroid, low bp, low glucose, fatigue, irregular HR, breast shrinkage

246
Q

Complications of sheehan’s syndrome?

A

Adrenal crisis, hypotension, unintended wt loss, menstrual irregularities

247
Q

Management of sheehan’s syndrome?

A

Lifelong hormone replacement eg corticosteroids, levothyroxine, oestrogen, GH

248
Q

When do baby blues occur?

A

During first week after childbirth, last for only a few days

249
Q

Timing of post-partum depression?

A

Depressive episode within first 12 months postpartum. Peak incidence during first 2 months

250
Q

Presentation of post partum depression?

A

Similar to symptoms of regular depression, negative cognitions about motherhood, anxiety surrounding baby

251
Q

Management of post partum depression?

A

Social support and psychological therapies
If not breastfeeding can use SSRI as usual, if breastfeeding need to weigh up risk benefit ratio with patient

252
Q

Timing of puerperal psychosis?

A

Can develop rapidly over a few hours and starts within days-weeks of delivery

253
Q

Who is puerperal psychosis more common in?

A

Those with bipolar affective disorder or other psychotic illness history.
Those with previous postpartum psychosis have 50% chance of recurrence in next pregnancy
FH links
NB/ can develop in women with no past psychiatric history too

254
Q

How to manage puerperal psychosis?

A

Most nee to be treated under MHA
Antipsychotic and/or mood stabiliser

255
Q

Prognosis of puerperal psychosis?

A

Good!
Most take 6-12 months to recover fully
Earlier diagnosis and intervention improves prognosis further

256
Q

Causes of puerperal infection?

A

Most= staph and strep
Highest risk in non-scheduled C section

257
Q

What is the leading cause of maternal mortality

A

VTE in pregnancy (about 1/3 of maternal deaths)

258
Q

Why is there increased risk of VTE in pregnancy?

A

Changes in protein levels in clotting cascade- increased fibrinogen and decreased protein S
Changed more pronounced as pregnancy progresses (highest risk is post partum)

259
Q

RFs for VTE in pregnancy?

A

Pre-existing RFs: thrombophilia, medical co-morbidities, age over 35, BMI over 30, parity over 3, smoking, varicose veins, paraplegia

Obstetric RFs: multiple pregnancy, pre-eclampsia, c-section, prolonged labour, stillbirth, preterm, PPH

260
Q

What investigations for VTE in pregnancy?

A

Bloods, compression duplex USS, ECG, CXR then CTPA or V/Q scan
NB/ d-dimer raised anyway in pregnancy so don’t test this

261
Q

Management of VTE in pregnancy?

A

LMWH throughout pregnancy until 6-12 weeks post partum
DON’T use warfarin as teratogenic
Prophylaxis if at least 4 RFs during assessment with LMWH

262
Q

How would amniotic fluid embolism present?

A

Acutely- hypoxia, resp arrest, hypotension, foetal distress, seizures, shock, confusion, cardiac arrest, DIC

263
Q

How is a definitive diagnosis of amniotic fluid embolism made?

A

On post mortem- foetal squamous cells and debris in pulmonary vasculature

264
Q

Levels of Hb for anaemia diagnosis in different trimesters?

A

First: Hb<110g/L
Second/third: Hb<105g/L
Postpartum: Hb<100g/L

265
Q

Why is anaemia likely in pregnancy?

A

In pregnancy, plasma volume and RBC mass increase but plasma volume increases disproportionately, so there is a haemodilution effect

266
Q

When do you screen for anaemia in pregnancy?

A

Screen at booking visit and at 28 weeks
Need to add in 20-28 week screen for multiple pregnancies

267
Q

Management of anaemia in pregnancy?

A

Trial of oral iron (1st line management and diagnostic test)
or folate supplementation

268
Q

When does rhesus disease of the newborn occur and why?

A

In rhesus negative mums with rhesus positive foetuses
Mum is sensitised to rh positive blood and then produces antibodies which will come into effect on second exposure
Antibodies cross the placenta and attack the foetal RBCs

269
Q

How will rhesus disease of the newborn/haemolytic disease of foetus and newborn present?

A

Haemolytic anaemia, jaundice, may have hypotonia, lack of energy
Symptoms may not develop until a few months of age

270
Q

What tests can be used to determine if there will be haemolytic disease of foetus?

A 
Kleihauer test (see if foetal blood in maternal circulation) 
Rosette test (incubate rh neg maternal sample with anti-Rh)
271
Q

How to prevent/decrease risk of haemolytic disease of newborn?

A

Anti-D to mum and monitoring

272
Q

UTI in pregnancy, which abx?

A

Nitrofurantoin is 1st line, but should be avoided at term: 100mg bd 1/52
2nd line= amoxicillin 500mg tds 1/52 or cefalexin 500mg bd 1/52

273
Q

What percentage of pregnant women carry GBS?

A

25%

274
Q

What can GBS cause? Name of pathogen

A

S. agalactiae
Can cause GBS disease of newborn, chorioamnioitis, endometritis

275
Q

How does chorioamniotis present?

A

Fevers, lower abdo tenderness, foul discharge, tachycardia

276
Q

How does endometritis present?

A

Fevers, lower abdo pain, intermenstrual bleeding, foul discharge

277
Q

How will a neonatal GBS infection present?

A

Pyrexia, cyanosis, resp difficulties, floppiness

278
Q

How to prevent poor outcomes in GBS positive women?

A

IV penicillins throughout labour in women (if GBS positive, UTI by GBS, previous baby with GBS, pyrexia during labour, premature, rupture membranes over 18 hours)

279
Q

When is management for GBS not indicated?

A

Elective C-section- as no rupture of membranes

280
Q

What are the risks of having a gonorrhoea infection during pregnancy?

A

Perinatal mortality, spontaneous abortion, premature labour, early foetal membrane rupture, vertical transmission causing conjunctivitis in foetus- which if untreated can cause long term blindness and damage

281
Q

What is cephalopelvic disproportion?

A

Mismatch between size of foetal head and maternal pelvis causing a difficulty in safe passage through the birth canal

282
Q

How to classify cephalopelvic disproportion? Examples for each

A 
Absolute CPD=true obstruction- permanent/maternal factors (contracted pelvis, pelvic exostoses, spondylolisthesis, tumours) or temporary/foetal factors (hydrocephalus, macrosomia) 
Relative CPD (brow/face presentations, occipitoposterior positions, deflexed head)
283
Q

Most common cause of cephalopelvic disproportion?

A

Contracted pelvis with average sized infant

284
Q

Management of cephalopelvic disproportion?

A

Depends when discovered
May have planned C section
May trial a vaginal delivery

285
Q

What can cause a hypoactive uterus/uterine inertia?

A

Premature labour, multiple pregnancy: over distension, psychology, contracted pelvis/malpresentation/deflexed head, full bladder, loaded rectum, hypertensive, anaemia/chronic illness, uterine fibroid

Primary or secondary inertia (after a period of good contraction)

286
Q

Complications of uterine inertia?

A

Prolonged labour, distress, increased risk of infection, PPH

287
Q

Management of uterine inertia?

A

Empty bladder and bowels, oxytocin, may need C section, can use instrumental delivery if head low enough

288
Q

Define obstructed labour?

A

Labour dystocia- baby doesn’t exit pelvis due to being physically blocked despite the uterus contracting normally

289
Q

Causes of obstructed labour?

A

cephalopelvic disproportion due to small pelvis/large baby/foetal malpresentation/tight perineum/abnormalities

290
Q

Complications of obstructed labour?

A

Foetal anoxia, pressure necrosis, foetal death, vesicovaginal fistula

291
Q

Management of obstructed labour?

A

Prevention is key!
Mode of delivery chosen on a case by case basis- episiotomy, ventouse, forceps, symphysiotomy, C section

292
Q

How can shoulder dystocia occur?

A

After delivery of head, anterior shoulder becomes impacted on maternal pubic symphysis (more common) or posterior shoulder impacted on sacral promontory

293
Q

RFs for shoulder dystocia?

A

Pre-labour RFs: previous event, macrosomia, diabetes, BMI over 30, induction of labour
Intrapartum RFs: prolonged 1st stage of labour, secondary arrest, prolonged 2nd stage, augmentation with oxytocin, assisted vaginal delivery

294
Q

Ultimate complication of shoulder dystocia?
Other complications

A

Delay in delivery of foetal shoulders causes hypoxia (proportional to time delay)
Others=tears (3rd and 4th degree), PPH, foetal fracture, brachial plexus injury

295
Q

Signs of shoulder dystocia?

A 
Failure of restitution (foetus doesn't turn to look to the side) 
Turtle neck (head retracts back into pelvis and neck no longer visible)
296
Q

Management of shoulder dystocia?

A

Stop pushing
Avoid downwards traction on foetal head (risk of brachial plexus injury)
Consider episiotomy
Use manoeuvres: McRoberts (hyperflex maternal hips and stop pushing, 90% success rate), suprapubic pressure (sustained or rocking fashion to apply pressure behind anterior shoulder)

Other 2nd line manoeuvres= internal rotation or posterior arm

297
Q

What is cord prolapse and types of it?

A

Umbilical cord descends through cervix with/before presenting part of foetus
Occult (incomplete-with foetus but not beyond)
Overt (complete-lower than presenting part in pelvis)

298
Q

Why does a prolapsed cord cause foetal hypoxia?

A

Occlusion of umbilical cord and arterial vasospasm due to cold exposure

299
Q

RFs for cord prolapse?

A

Breech presentation, unstable lie, artificial rupture of membranes, polyhydramnios, prematurity, PROM, long cord, multiple pregnancy

300
Q

How to manage cord prolapse?

A

Avoid handling of cord to reduce vasospasm, manually elevate the presenting part, encourage into left lateral position, consider tocolysis (stop contraction), emergency C-section/quickest mode of delivery

301
Q

What is lie of foetus? What are potential lies of the foetus? what’s normal?

A

Lie=relationship between long axis of foetus and mother
Longitudinal, transverse, oblique
Longitudinal is lie if the right way up!

302
Q

What is presentation of the foetus? What types?

A 
Presentation= foetal part that first enters the maternal pelvis 
Cephalic vertex (most common and safest), breech, shoulder, face, brow
303
Q

What is foetal position? What types?

A

Position of foetal head as it exits birth canal
Occipito-anterior (ideal), occipito-posterior or occipito-transverse

304
Q

How to manage abnormal foetal lie?

A

External cephalic version (ECV) between 36 and 38 weeks to manipulate foetus to a cephalic presentation through maternal abdomen

305
Q

Who can’t you do ECV in?

A

Recent APH, ruptured membranes, uterine abnormalities, previous C section

306
Q

How to manage abnormal foetal position?

A

90% of malpositions spontaneously rotate as labour progresses
If not, rotation and operative vaginal delivery or C section

307
Q

How to manage malpresentations?

A

Brow or shoulder- need C section
Face : if chin anterior can have normal labour, but likely to be prolonged, if chin posterior need C section

308
Q

Types of breech presentation?

A

Complete (flexed, cross legged appearance)
Frank (extended- flexed at hip and extended at knee)- most common
Footling (extended at knees)

309
Q

Management of breech presentation?

A

About 28% babies breech at 28 weeks but only 3% at term, use USS to confirm diagnosis
ECV, if unsuccessful then C-section (vaginal breech birth can be attempted but requires specific manoeuvres)

310
Q

Complications of breech presentation?

A

Cord prolapse, foetal head entrapment, prem rupture of membranes, birth asphyxia, intracranial haemorrhage

311
Q

Types of instrumental delivery/operative vaginal delivery?

A

Forceps
Ventouse (silastic cup for occipito-anterior or kiwi cup for any position)

312
Q

Indications for instrumental delivery?

A

Inadequate progress, maternal exhaustion, maternal conditions where prolonged exertion should be limited, suspected foetal compromise, any clinical concerns

313
Q

When should you stop using instrumental delivery?

A

After 3 contractions and pulls with any instruments with no reasonable progress, should abandon attempt

314
Q

Pros and cons of ventouse?

A

Lower success rate, increased foetal injury eg retinal haemorrhage, must be over 34 weeks to attempt
Lower incidence of maternal injuries, less pain

315
Q

Pros and cons of forceps?

A

Higher success rate, no maternal effort required
Higher rate of tears

316
Q

Contraindications to instrumental delivery?

A

Incomplete dilation, true CPD, breech/face/brow presentation, can’t be under 34 weeks for ventouse

317
Q

Potential complications of instrumental delivery?

A

Jaundice, lacerations, haematoma, facial nerve damage, fractures, tears, VTE, incontinence, PPH, shoulder dystocia, infection

318
Q

What is polyhydramnios?

A

Amniotic fluid above 95th centile for gestational age

319
Q

Causes of polyhydramnios?

A

Idiopathic in 50-60%
Other cases= foetal swallow prevention, duodenal atresia, anaemia, foetal hydrops, twin-twin transfusion syndrome, increased lung secretions, genetic abnormalities, maternal diabetes, maternal lithium ingestion, macrosomia, some TORCH infections

320
Q

How to diagnose polyhydramnios or oligohydramnios?

A

On USS using either amniotic fluid index or maximum pool depth

321
Q

Management of polyhydramnios?

A

Most don’t need management, good prognosis
May consider amnioreduction or indomethacin (enhances water retention)

322
Q

What is oligohydramnios?

A

Low level of amniotic fluid, less than the 5th centile for gestational age

323
Q

What causes oligohydramnios?

A

Anything that reduces production of urine, blocks output from foetus, or ruptures the membranes
Main causes= preterm premature rupture of membranes, placental insufficiency, renal agenesis (Potter’s syndrome), non functioning foetal kidneys, obstructive uropathy, genetic/chromosomal anomalies, viral infections

324
Q

What test to do if considering ruptured membranes as the cause of oligohydramnios?

A

IGFBP-1 in vagina (bedside test)

325
Q

How to manage oligohydramnios?

A

Manage underlying cause
Ruptured membranes- labour likely to commence within 24-48 hours, consider induction, need steroids and abx
Placental insufficiency- likely to be delivered before 36/37 weeks

326
Q

Prognosis of oligohydramnios in 2nd trimester?

A

Poor
Decreased amniotic fluid means decreased foetal movements, which causes muscle contractures

327
Q

Pathophysiology of pubic symphysial dysfunction?

A

Physiological pelvic ligament relaxation and increased joint mobility in pregnancy causes discomfort and pain in pelvic area, may radiate to upper thighs and perineum

Joint sufficiently relaxed to allow instability in pelvic girdle- excessive movement of pubic symphysis in anterior or lateral direction

328
Q

What other factors apart from pregnancy itself can contribute to pubic symphysial dysfunction?

A

Strenuous work during pregnancy, weight gain, multiparity, increasing age, history of difficult deliveries

329
Q

Presentation of pubic symphysial dysfunction?

A

PAIN- variable, usually relieved by rest, disappears commonly after giving birth
LOCOMOTOR difficulties- walking, stairs, chairs, weight bearing activities, turning in bed, standing on one leg

330
Q

How to manage pubic symphysial dysfunction?

A

Analgesia (paracetamol) then after delivery can use NSAIDs
Weight-bearing aids, physio and exercise

331
Q

When do multiparous women have appointments in antenatal schedule?

A

GP contact, 8-12 week booking and 8-14 week dating scan
16 weeks, 20 week anomaly scan, 28 weeks, 34 weeks, 36 weeks, 38 weeks

332
Q

What extra appointments do nulliparous women get in antenatal schedule?

A

25 weeks, 31 weeks, 40 weeks

333
Q

What sorts of things are done in antenatal schedule?

A

(Sickle cell/thalassaemia screening offered before 10 weeks)
BP, urine, screening, measure uterus, care plan, any anti-D injections, information giving, checking position of foetus, ECV if required

334
Q

What may be discussed at 41 week appointment?

A

Offer a membrane sweep, discuss induction

335
Q

What is looked at in the 20 week/anomaly scan?

A

Looks at bones, heart, brain, spinal cord, face, kidneys, abdomen and can determine sex

336
Q

What 11 conditions does the 20 week scan look for?

A

Anencephaly, open spina bifida, cleft lip, diaphragmatic hernia, gastroschisis, exophthalmos, serious cardiac abnormalities, bilateral renal agenesis, lethal skeletal dysplasia, Edward’s syndrome (trisomy 18), Patau’s syndrome (trisomy 13)

337
Q

How are the trisomies screened for?

A

Combined test (USS and blood test) then nuchal translucency measurement at 12 week scan

For trisomy 21, can do quadruple blood screening test iif combined not done- done at 14-20 weeks

338
Q

At what point is routine anti-D prophylaxis given?

A

28 and 34 weeks

339
Q

Different types of breast cancer?

A

Ductal carcinoma in situ, invasive lobular carcinoma, angiosarcoma, inflammatory breast cancer, lobular carcinoma in situ, male breast cancer, Paget’s disease of the breast, recurrent breast cancer

340
Q

How will breast cancer present?

A

Lump/thickening, change in size/shape/appearance, skin changes, newly inverted nipple, peeling/scaling/crusting of areola or breast, redness or pitting

341
Q

RFs for breast cancer?

A

BRCA1/2, female, increasing age, history of breast condition, previous breast cancer, family history, genes, radiation exposure, obesity, puberty under 12, menopause over 55, first child at older age, nulliparous, postmenopausal HRT, alcohol

342
Q

What is involved in triple assessment of breast cancer?

A

Breast examination
Mammogram/USS
Biopsy

343
Q

How is breast cancer managed?

A

Depends on stage and prognosis
Surgery (lumpectomy, mastectomy, sentinel node biopsy, axillary LN dissection, prophylactic mastectomy)
Radiation, chemo, hormone therapy

344
Q

What hormone therapies may be used in breast cancer?

A

Selective oestrogen receptor modulators/SERMs eg tamoxifen
Aromatase inhibitors eg anastrozole
Surgery/medication to suppress ovaries

345
Q

When is breast screening undertaken?

A

Every 3 years between 50 and 70 years

346
Q

When are implants allowed on the NHS?

A

Severe asymmetry or amastia

347
Q

2 types of breast implants with pros/cons

A

Silicone- most common, less likely to rupture, more natural, can spread into breast and cause lumps
Saline- more likely to fold/rupture/go down over time, but will be absorbed safely into the body

348
Q

What is the earliest form of breast cancer?

A

In situ carcinoma- abnormal cells inside milk duct

349
Q

Presentation of paget’s disease of the nipple

A

Flaky/scaly nipple, crusting/oozing/hardened skin, itch, erythema, tingling/burning sensation, inverted/flattened nipple, lump
Usually unilateral

350
Q

3 common benign breast lumps?

A

Breast abscess, cysts, fibroadenoma (most common)

351
Q

Two kinds of breast abscess?

A

Lactational-peripheral region of breast, commonly upper and outer quadrant
Non lactational-central/subareolar or lower quadrants

352
Q

Risk factors for breast abscess?

A

Previous mastitis, immunosuppressed, S. aureus carriage, poor hygiene

353
Q

How will breast abscesses present?

A

Recent history mastitis or previous abscess, fever, general malaise, painful swollen lump, inflammatory signs
Lump may be fluctuant with skin discolouration

354
Q

How to manage breast abscess?

A

Diagnose by USS.
Drainage then culture fluid to guide abx choice, advise lactating women to continue breastfeeding

355
Q

How do breast cysts present?

A

Smooth and mobile, round/oval lump
May have nipple discharge (clear/yellow/brown)
Pain/tenderness over area
Increased size/tenderness just before period
Symptoms improve after period

356
Q

Do breast cysts require treatment?

A

Generally no

357
Q

Different types of fibroadenoma?

A

Simple, complex, juvenile, giant (over 2 inches), phyllodes tumour (risk of becoming malignant)

358
Q

How does a fibroadenoma present?

A

Most often in 15-35 year olds
Round, distinct smooth borders, easily moved, firm or rubbery, painless lump
Lumps can become bigger during pregnancy/use of hormone therapy, might shrink after menopause

359
Q

What swabs in double swab? Triple swab?

A 
Double= NAAT then high vaginal charcoal media 
Triple= NAAT, then high vaginal charcoal media and endocervical charcoal media swab
360
Q

What does NAAT swab detect for? Where to swab?

A

Swab endocervical or vulvovaginal
Detects chlamydia and gonorrhoea

361
Q

What does a charcoal media swab detect? Where to swab?

A

High vaginal swab
Detects BV, trichomonas vaginalis, candida, GBS

362
Q

RFs for vulvovaginal candidiasis?

A

Pregnancy, diabetes, broad spectrum abx, corticosteroids, immunocompromised

363
Q

How does thrush present?

A

Pruritus vulvae, discharge (white, curd like, non offensive), dysuria (superficial), erythema and swelling of vulva, satellite lesions (red, pustular with superficial white/creamy pseudomembranous plaques that can be scraped off)

364
Q

How to manage thrush?

A

No need to investigate if uncomplicated
Initial pessary antifungal eg clotrimazole (pregnancy= only option, don’t use oral)
Consider oral antifungal eg fluconazole
Topicla imidazole in conjunction to address vulval symptoms
If symptoms persisting over 7-14 days, need to review
If recurrent/ complicated- need vaginal smear and microscopy

365
Q

Organism causing chlamydia? Incubation period?

A

Chlamydia trachomatis (bacterium). 7-21 days incubation

366
Q

Presentation of chlamydia?

A

70% women asymptomatic, 50% men asx
Dysuria, abnormal discharge, intermenstrual/postcoital bleeding, dyspareunia, lower abdo pain, cervicitis +/- contact bleeding, mucopurulent endocervical discharge, pelvic tenderness, cervical excitation

367
Q

Investigations for chlamydia?

A

National screening for sexually active under 25s
Vulvovaginal swab then for NAAT (endocervical swab or 1st urine catch are 2nd line alternatives)

368
Q

How to manage chlamydia?

A

Doxycyline orally 100mg bd for 1 week
or
stat azithromycin 1g
Avoid sex until treatment completed, partner tracing

369
Q

How does bacterial vaginosis present?

A

50% asx,
Discharge: Offensive, fishy smelling, white/grey, thin
Not usually associated with irritation
Vaginal pH more than 4.5

370
Q

Pathophysiology of BV?

A

some disturbance in natural vaginal flora, causes a decrease in lactobacilli. This increases the pH and allows a polymicrobial infection- especially Gardnerella vaginalis, anaerobes and mycoplasma

371
Q

RFs for BV?

A

sex, IUD, receptive oral sex, STI present, douching, recent abx, smoking, black

372
Q

Investigating for BV?

A

High vaginal smear and microscopy
Can do vaginal pH over 4.5
Can do KOH whiff test (alkali added causing strong fishy odour)

373
Q

Management for BV?

A

oral metronidazole 400mg bd for 5-7 days or stat 2g
Can use topical gel

374
Q

What causes trichomoniasis?

A

Curable STI by protozoan Trichomonas vaginalis

375
Q

Presentation of trichomoniasis?

A

Commonly asx, offensive vaginal odour, abnormal discharge (yellow-green), vulval irritation, dyspareunia, dysuria, vulvitis, strawberry cervix

376
Q

Management of trichomoniasis?

A

Metronidazole- 2g stat or 400-500mg bd for 5-7days
Partner trace (preceding 4 weeks)
Abstain from sex until treatment completed

377
Q

Cause of gonorrhoea?

A 
Neisseria gonorrhoea (bacteria)
-gram negative diplococci
378
Q

Presentation of gonorrhoea?

A

Around 50% asx, sxs occru 2-5 days after infection, altered/increased discharge (thin, watery, green or yellow), dysuria, dyspareunia, lower abdo pain, rarely causes unexpected bleeding

Often co-exists with chlamydia infection

379
Q

Management of gonorrhoea?

A

IM ceftriaxone 1g and partner notification

380
Q

Which herpes causes what?

A 
HSV-1= genital herpes and cold sores 
HSV-2= genital herpes
381
Q

How will a primary HSV infection present?

A

Small red blisters- very painful and can form open sores, discharge, flu like symptoms, itchy genitals
After 20 days lesions crust and heal

382
Q

How will secondary HSV infections present?

A

Recurrent outbreaks (shorter and less severe over time), burning and itching, red blisters

383
Q

How long do cold sores last?

A

7-10 days

384
Q

How to investigate and manage HSV infection?

A 
Ix= swab open sore and send for PCR 
Mx= aciclovir and full STI screen
385
Q

What causes syphilis?

A

STI caused by spirochete gram negative bacteria Treponema pallidum

386
Q

Presentation of primary syphilis?

A

Bacteria divide forming infectious hard ulcer= chancre forming after 2-3 weeks

Papule>chancre (painless)
Heal within 3-10 weeks, can persist during secondary syphilis

NB/ if chancre left untreated, systemic damage via obliterating arteritis causes ischaemia and symptoms

387
Q

How does secondary syphilis present?

A 
3 months post initial infection 
Skin rash (hands and feet), fever, malaise, arthralgia, wt loss, headaches, condylomata lata, painless lymphadenopathy, silver mucous membrane lesion
388
Q

How does tertiary syphilis present?

A

Gummatous (non infectious, various tissues)
Neurosyphilis (tabes dorsalis, dementia, meningovascular complications, argyll robertson pupil)
Cardiovascular (aortic regurgitation, angina, calcification of ascending aorta)

389
Q

How to investigate syphilis?

A

Dark ground microscopy, PCR, serology, LP (?neuro)

390
Q

How to manage syphilis?

A

Penicillin (benzathine)

391
Q

What may happen 24 hours after treatment of syphilis?

A

Jarisch Herxheimer reaction- flu like illness
Needs follow up serology

392
Q

What causes genital warts?

A 
Human papillomavirus (mainly HPV 6 and 11) 
Needs skin-skin contact
393
Q

How to manage genital warts?

A

May not need tx
Topical tx eg podophyllotoxin/imiquimod
Physical ablation (excision, cryotherapy, electrosurgery, laser surgery)
Vaccination!

394
Q

Describe progression of HIV to AIDS

A

Single stranded RNA retrovirus uses CD4 cells
Seroconversion (producing anti-HIV abs), flu like illness with decreasing CD4 levels- highly infectious
Latent phase- decreasing Cd4 and increasing viral load
May be asx latent phase initially, then late latent= infectious
Over 10 years or so, becomes AIDS when CD4 is under 200

395
Q

What investigations for HIV/AIDS?

A

4th generation tests- HIV antibodies and p24 antigen

396
Q

How to manage HIV?

A

HAART reduces viral load to undectable (=untransmissable) levels, but not a cure- atripla, eviplera etc
PEP if within 72 hours of contact and taken for a month (truvada and raltegravir)

397
Q

Pregnant woman with HIV- what to do and what does t reduce risk of transmission to?

A

Antenatal HAART, avoid breastfeeding, neonate PEP
Reduced risk from over 25% to less than 1%

398
Q

4 phases of sexual arousal?

A

Excitement, plateau, orgasmic, resolution

399
Q

What happens in excitement phase in men?

A

Psychogenic or somatogenic stimuli

Sacral parasympathetic
Arteriolar vasodilation in corpora cavernosa, penile filling (latency) and penile tumescence (erection)

400
Q

What happens in plateau phase in men?

A

Sacrospinous reflex
Contraction of ischiocavernosus, venous engorgement and decreased arterial inflow, testes engorged and elevated
Secretion from accessory glands (5% ejaculate), lubricates distal urethra and neutralises acidic urine
Increased HR and BP

401
Q

What happens in orgasmic phase in men?

A 
Emission= thoracolumbar sympathetic reflex- contraction of smooth muscle, internal and external urethral sphincters contract, semen pools in urethral bulb (mixing of ejaculate contents) 
Ejaculation= spinal reflex (l1, l2), contraction of glands and ducts and urethral sphincter, filling internal urethra stimulates pudendal nerve- contracts genital organs and expels semen
402
Q

What happens in resolution phase in men?

A

Thoracolumbar sympathetic- contraction of arteriolar smooth muscle, increased venous return, causes dehumescence flaccidity and refractory period

403
Q

Nervous system control of female 4 phases of sexual arousal?

A 
Excitement= sacral parasympathetic 
Plateau= sacrospinous reflex 
Orgasmic= thoracolumbar sympathetic reflex and spinal reflex 
Resolution= thoracolumbar sympathetic
404
Q

Describe excitement phase in women?

A

Vasocongestion, vaginal lubrication, clitoris engorges, uterus elevates, increased muscle tone/HR/BP, inner 2/3 of vagina lengthens and expands

405
Q

Describe plateau phase in women?

A

Increased tone/HR/BP, labia minora deepends in colour, clitoris withdraws under hood, bartholin glands secretion to lubricate vestibule, uterus completely elevated and orgasmic platform forms in lower 1/3 of vagina

406
Q

Describe orgasmic phase in women?

A

Orgasmic platform contracts rhythmically 3-15 times, uterus and sphincter contracts

407
Q

Describe resolution phase in women?

A

Clitoris descends, labia return to normal size and colour, uterus descends, vagina shortens and narrows, no refractory period

408
Q

What happens to aid the sperm to reach the ampulla for fertilisation?

A

Oxytocin stimulates uterus to contract aiding travel
Sperm undergoes capacitation- tail movement changes from beat like action to thrashing whip like action, also removal of protein coat of sperm exposes the acrosome enzymes which allows penetration of zona pellucida

409
Q

Physiology of sperm fertilising the ovum

A

After capacitation, zona pellucida 3 (ZP3) proteins interact with sperm and allow calcium to enter spermatozoa, causing increased cAMP
Acrosome swells, outer membrane fuses with sperm plasma membrane- releases enzymes
Inner cell membrane of acrosome exposed, ZP2 glycoprotein holds sperm near egg
Proteolytic enzymes penetrate ZP and sperm and oocyte membranes fuse and calcium enters cells stopping them moving

410
Q

What prevents polyspermy?

A

Calcium enters, egg cell membrane depolarises (primary block preventing polyspermy)
Cortical reaction where granules in egg release contents into ZP (secondary block to polyspermy)
Final meiotic division (polar body released)

411
Q

How does the placenta form?

A

Formed form outer trophoblast cells
Day 9- lacunae/spaces form within syncytiotrophoblast and this erodes maternal tissues allowing maternal blood from uterine spiral arteries to enter the lacunar network
Cytotrophoblast forms primary chorionic villi which penetrate and expand into syncytiotrophoblast, by 3rd week secondary chorionic villi form
Villi expand into branching villi to form surface area for exchange

412
Q

How does the placenta change throughout trimesters?

A

First= thick placental barrier
By full term= increased surface area but barrier much thinner and cytotrophoblast layer is lost from first trimester

413
Q

What is the placenta covered by on maternal and foetal side?

A 
Maternal= decidua basalis 
Foetal= chorionic plate
414
Q

at 4/5th month, what happens to placenta?

A

Decidua form decidual septa- divides placenta into cotyledons, where each receives blood supply from 80-100 spiral arteries

415
Q

What does the placenta like by full term?

A

Discoid, 15-25 cm diameter, 3cm thick, weighs about 500g
Maternal side has about 15-20 bulging areas

416
Q

What score can be used to judge likelihood of woman entering labour soon?

A

Bishop scoring

417
Q

What factors are considered in bishop scoring?

A

Dilation, effacement (how thin cervix is), consistency (should be a soft cervix), position (cervix should move forward with head), foetal station (how far up baby’s head is)

418
Q

What different bishop scores mean?

A

Over 8= spontaneous labour about to start soon
6 or 7= unlikely to start soon, induction of labour could go either way
Under 5= unlikely and induction probably won’t work

419
Q

What is a partogram?

A

Document used to monitor labour
Records maternal obs, foetal HR, amniotic fluid, contraction frequency and strength, position, cervicograph, any oxytocin administration, urine, all vaginal examinations

420
Q

What does cardiotocography measure?

A

Foetal HR and contractions

421
Q

How can CTG be performed?

A

External maternal elastic belt
Can insert vaginal electrode for FHR

422
Q

Indications for CTG?

A

Premature/smaller than expected, htn, fever, infection, fresh blood passed in labour, multiple pregnancy, passed meconium, premature rupture of membranes, unusual foetal position, labour sped up or epidural needed

423
Q

What are foetal scalp samples?

A

Used during labour to confirm foetal oxygenation
Create shallow cut by a transvaginally inserted blood lancet
Tests pH and lactate as acidosis a/w hypoxia

424
Q

When would you do a foetal scalp sample?

A

If CTG suggested pathology

425
Q

Indications for amniocentesis?

A

Genetic testing eg trisomy 21
Foetal lung testing- if mature enough for birth (32-39 weeks)
Diagnosis of foetal infection
Evaluate severity of anaemia in babies with Rh sensitisation
Polyhydramnios treatment
Paternity testing

426
Q

When is genetic amniocentesis performed?

A

Between 15-20 weeks

427
Q

Risks of amniocentesis?

A

Leaking amniotic fluid, miscarriage, needle injury, Rh sensitisation, infection, infection transmission

428
Q

When is chorionic villus sampling done?

A

Usually between 11-14 weeks, but can be done as early as 10 weeks

429
Q

What can chorionic villus sampling not detect?

A

Neural tube defects (but genetic amniocentesis can)

430
Q

Cons of chorionic villus sampling?

A

Risks of miscarriage, rh sensitisation and uterine infection
Sometimes results are unclear and may need amniocentesis as well
Rare chance of false positive

431
Q

What is viability re ejaculate, and the usual number?

A

What percentage of live sperm are in a semen sample
Should be at least 58%

432
Q

Examples of fertility medications?

A

Clomifene (encourages ovulation in women who ovulate irregularly)
Tamoxifen (alternative to clomifene)
Metformin (if has PCOS)
Gonadotrophins
GnRH and dopamine agonists (encourgae ovulation)

433
Q

Options for assisted conception?

A

Fertility medications
Fertility surgery (fallopian tubes if blocked or scarred, laparoscopy for endometriosis)
Intrauterine/artificial insemination
In vitro fertilisation
Donation (egg or sperm)

434
Q

Causes of male infertility?

A

Low sperm production, abnormal sperm function, blockages
Medical eg varicocele, infection, retrograde ejaculation, antibodies, tumours, undescended testes, hormones, tubule defects, chromosome, sex problems, Coeliac, medications, prior surgery
Environmental eg industrial chemicals, heavy metal, radiation, overheated testes
Lifesyle eg drug abuse (anabolic steroids, cocaine, weed), alcohol, smoking, obesity

435
Q

What is the apgar score?

A

Describes condition of newborn infant immediately after birth done at 1 minute and 5 minutes

Activity (tone), pulse, grimace (reflex irritability), appearance (colour), respiratory

436
Q

What apgar score means hypoxia-ischaemia is unlikely?

A

Over 7 at 5 minutes

437
Q

2 types of HRT? 2 regimes?

A

Combined or oestrogen only (for hysterectomy patients)
Regimes= cyclical or continuous

438
Q

SEs of HRT?

A

Oestrogen and progestogen related= bloating, breast tenderness, nausea, cramps, headaches, vaginal bleeding
Progestogen related= mood swings, depression, acne, abdo pain, back pain

439
Q

What defines heavy menstrual bleeding?

A

Subjectively (what the woman deems) heavy

440
Q

Causes of menorrhagia?

A

Most due to a combination of coagulopathy, ovulatory and endometrial dysfunction
Pathological causes=uterine fibroids (20-30%), polyps (5-10%), endometriosis
40-60% women= dysfunctional uterine bleeding

441
Q

NICE investigation for menorrhagia?

A

FBC +/- haematinics, coagulation, TFT, TVUS, hysteroscopy +/- endometrial biopsy

442
Q

Management options for menorrhagia/abnormal uterine bleeding?

A 
1= IUS (Mirena) 
2= antifibrinolytics eg transexamic acid 
3= NSAIDs eg mefenamic acid 
4= progestogens eg medroxyprogesterone acetate or northesisterone 
5= COCP 
6= POP 
7= danazol 
8= reassurance 
9= endometrial ablation 
10= hysterectomy 
11= uterine artery embolisation 
12= myomectomy/resection fibroids
443
Q

Example of antifibrinolytic and administration? how does it work?

A

Transexamic acid 1g TDS for up to 4 days

Inhibits tissue plasminogen activator

444
Q

How does mefenamic acid work? administration?

A

inhibits COX and blocks PGE2 receptors

500mg tds until bleeding stops/reduces

445
Q

When are progestogens least effective in AUB? When must you use them? How long to take them for? 2 examples?

A

Least effective if in luteal phase. Should use from day 5-25. Take for minimum 3 months

Medroxyprogesterone acetate and northesisterone

446
Q

How does danazol work?

A

Inhibits sex steroid production and blocks receptors

447
Q

Indications for endometrial ablation?

A

HMB, not expecting amenorrhoea, normal endometrium, uterus under 12 weeks size, completed family

448
Q

Contraindications to endometrial ablation?

A

Malignancy, acute PID, desire for future pregnancy, excessive uterine cavity length

449
Q

Which options for AUB are fertility sparing?

A

Uterine artery embolisation and myomectomy/resection of fibroid

450
Q

What time period= puerperium?

A

From delivery of placenta to 6 weeks following the birth

451
Q

During involution of uterus and genital tract in puerperium, what different lochia are shed?

A

Lochia rubra (day 0-4), lochia serosa (day 4-10), lochia alba (day 10-28)

452
Q

Describe prolactin response in breast feeding?

A

Baby suckles, sensory impulses from nipple to brain, prolactin from anterior pituitary via bloodstream to breasts, makes lactocytes produce milk

More secreted at night, suppresses ovulation, level peaks after feed (to produce milk for next feed)

453
Q

Describe oxytocin reflex in breast feeding?

A

Baby suckles, sensory impulse from nipple to brain, oxytocin released from posterior pituitary, causes myoepithelial cells to contract and expel milk

Helped by sight, sound and smell of baby, hindered by anxiety/stress/pain

454
Q

Benefits of breastfeeding?

A

Decreases GI disease, resp disease, otitis media and NEC in baby
Lactoferrin: regulated iron absorption and delivery, boosts immune system

455
Q

How does post dural puncture headache present?

A

Headache worse on sitting/standing, starts 1-7 days after spinal/epidural. Neck stiffness, photophobia

456
Q

RFs for urinary retention in puerperium?

A

Epidural analgesia, prolonged 2nd stage of labour, forceps/ventouse, extensive perineal lacerations, poor labour bladder care

457
Q

What is obstetric cholestasis?

A

Itching with no rash, abnormal liver function (increased AST, ALT and bile acid), resolves after delivery

458
Q

How to manage obstetric cholestasis?

A

Urseodeoxycholic acid

459
Q

Anti-thyroid drug to use in pregnancy?

A

Propylthiouracil

460
Q

When would you offer sickle cell and thalassaemia screening?

A

By 8-10 weeks in all pregnant women
Unbooked women in labour

461
Q

When are babies to hepatitis B woman vaccinated?

A

Within 24 hours of birth
4,8,12 and 16 weeks
Then at 12 months

462
Q

When is the combined test offered?

A

11+2 to 14+1 weeks

463
Q

What is involved in the combined test?

A

Uses maternal age, crown rump, nuchal translucency, 2 biochem markers= PAPP-A and free BHCG

464
Q

What can combined test screen for?

A

2 risk results produced
1 for T21
1 for T18/T13

465
Q

What is quadruple testing for? When to offer?

A

T21
14+2 to 20+0 weeks or when head circumference is 101-172mm

466
Q

What is involved in quadruple testing?

A

Alpha fetoprotein, total BHCG, oestriol and inhibin A

467
Q

When is the early pregnancy scan done, what for?

A

10-14 weeks
For dating and confirming viability, can form part of combined test

468
Q

When is foetal anomaly screening done?

A

18-20 week

469
Q

What does the foetal anomaly screening scan look for?

A

Open spina bifida, anencephaly, cleft lip, diaphragmatic hernia, gastroschisis, exomphalos, serious cardiac abnormalities, bilateral renal agenesis, lethal skeletal dsyplasia, trisomy 13+18

470
Q

When might transdermal patch HRT be used?

A

Gastric upset eg Crohns, need for steady absorption (eg migraines), perceived increased risk of VTE, older women, medical conditions eg htn, patient choice

471
Q

How to diagnose premature ovarian insufficiency?

A

In under 40
FSH over 25 IU/L in 2 samples 4 weeks apart and 4 months of amenorrhoea

472
Q

How fertile are you generally around menopause?

A

For 2yrs if menopause under 50 years
For 1 year if menopause over 50 years

473
Q

Contraindications to HRT?

A

Undiagnosed abnormal PV loss, breast lump, acute liver disease

474
Q

When should you use HRT with caution?

A

Fibroids, uncontrolled BP, migraine, epilepsy, endometriosis, FH VTE, over 60s

475
Q

Genes associated with breast cancer?

A

BRCA1/2, Tp53, PTEN, STKII, CDHI

476
Q

How to investigate a breast presentation?

A

Triple assessment: clinical exam, imaging, biopsy.
Everything scored 1-5.

477
Q

What is the nottingham prognostic index used for?
Formula?

A

Prognosis of breast cancer if no treatment other than surgery used

Grade (1-3) x nodes (1-3) + 0.2(size cm)

Score 2-7 with 7 being worst prognosis

478
Q

Receptors used in prognosis and treatment in breast cancer?

A

ER (positive= good)
PgR (positive=good)
Her2 (positive=bad)
Ki67 (positive=bad)

479
Q

Endocrine treatment options for breast cancer?

A

Direct oestrogen receptor inhibitor (pre menopausal)= tamoxifen

Aromatase inhibitors (stops androgen conversion to oestrogen) (post menopausal)= anastrazole, letrozole

480
Q

Adjuvants for breast cancer therapy?

A

Chemo, endocrine, trastuzumab/herceptin and pertuzumab (for Her2 +ve), radio, bisphophonates (decrease mets)

481
Q

What is non cyclical breast pain usually due to`?

A

Pulled pectoral or serratus muscle
RARELY due to cancer

482
Q

When can you carry out termination of pregnancy?

A

Before 24 weeks
After 24 weeks if risk to life of baby or if to prevent grave permanent injury to maternal physical/mental health, or if continuation of pregnancy would involve risks to life of pregnant woman

2 consultants need to sign

483
Q

Female genital mutilation type 1?

A

Clitoridectomy (partial or total)

484
Q

FGM type II?

A

Excision: clitoris and labia minora (partial or total)

485
Q

FGM type III?

A

Infibulation: narrowing of vaginal orifice with creation of a covering seal +/- clitoral excision

486
Q

FGM type IV?

A

All other harmful procedures including pricking, piercing, incising, scraping and cauterisation

487
Q

Difference between a uterine fibroid and a poylp?

A

Fibroid = benign tumour of fibrous muscle tissue

Polyp = benign tumour of endometrial tissue

488
Q

UK law on FGM?

A

Offence to perform, assist in carrying out, assist non UK person to carry out FGM outside of UK on UK national or permanent UK resident

489
Q

Hormones involved in labour?

A

Prostaglandins, oxytocin, oestrogen (surge at labour to inhibit progesterone to prepare smooth muscle), beta endorphins (natural pain relief), adrenaline (released as birth is imminent), prolactin

490
Q

What is the most common pelvis type in females? other types?

A

Gynaecoid most common

others= platypelloid, android, anthropoid

491
Q

Mechanism of labour?

A

Descent, flexion of neck, internal rotation, extension, external rotation (naturally aligns head with shoulders), delivery of body (anterior then posterior shoulder)

492
Q

How much amniotic fluid at term?

A

500-800mls

493
Q

What is the term used for when foetus born in intact amniotic sac?

A

en caul

494
Q

Why do we allow at least 1 minute before clamping the umbilical cord?

A

Allows time to transfuse blood to baby (can received up to 214g of blood), allows baby transition time to extra uterine life, increases rbcs/iron/stem cells, decreased need for inotropic support

495
Q

Analgesia options in labour?

A

Holistic and non invasive eg aromatherapy, water immersion, massage, TENS

Etonox (gas and air), paracetamol and codeine

Opioids: diamorphine, pethidine, remifentanyl

Epidural (mix of bupivacaine and fentanyl)

496
Q

2 planes for mammogram?

A

Craniocaudal (horizontal plates)- for medial breast and deeper parts

Medio-lateral oblique- good for axillary tail and lateral breast

497
Q

How much does breast cancer screening reduce mortality?

A

Between 16 and 29%

498
Q

Main two types of invasive breast cancer?

A

ductal (70%)
lobular (10%)- harder to feel, more diffuse, more prone to be bilateral

499
Q

On breast screening, what are ductal carcinomas in situ and how do they look on mammogram?

A

Pre-malignant, not yet able to invade basement membrane so can’t metastasise
Appear as microcalcifications generally

500
Q

Fluid and renal physiological changes in pregnancy?

A

Increased total plasma volume (30-50%)
Favour sodium retention and increase potassium absorption
Increased extracellular fluid; dilution effects
Decreased plasma osmolality without diuresis, decreased plasma oncotic pressure
Increase kidney size (20%)
Dilation of renal system, decreased ureteral tone
Increased renal blood flow, increased GFR
Increased renin-angiotensin II

501
Q

CV physiological changes in pregnancy?

A

Peripheral vasodilation early on, increased SV, HR, and CO
BP changes biphasic: early on drop in BP, increase in late pregnancy
Dilution anaemia, increased polymorphs
Hypercoagulable

502
Q

Resp physiological changes in pregnancy?

A

Diaphragmatic elevation
Increased maternal oxygen consumption
TLC, FRC, VC and ERV+IRV reduced
Increased TV increases minute volume

Maternal RBCs have increased 2,3 diphosphogylcerate (DPG)- allows o2 release at same po2

503
Q

GI physiological changes in pregnancy?

A

Progesterone induced generalised smooth muscle relaxation
decreased CCK and decreased gallbladder motility
Increased gut transit time

504
Q

Metabolic physiological changes in pregnancy?

A 
Weight gain (mean around 12.5kg) 
Early= maternal glycogen synthesis and fat deposition, late= maternal insulin resistance
505
Q

Which pessary will still allow sexual intercourse?

A

Ring

506
Q

Different types of hypertension to experience in pregnancy?

A

Gestational hypertension
Pre-eclampsia, eclampsia
Chronic hypertension
Pre-eclampsia superimposed upon chronic hypertension

507
Q

What defines gestational hypertension?

A

New hypertension after 20 weeks gestation
Systolic over 140 and or diastolic over 90mmHg
No or little proteinuria

508
Q

What counts as chronic hypertension with superimposed pre-eclampsia?

A

New onset proteinuria after 20weeks or before if there’s a sudden increase in proteinuria/BP, thrombocytopenia or abnormal AST/ALT

509
Q

What protein:creatinine ratio can be seen in pre-eclampsia?

A

Over 30mg/mmol

510
Q

What warrants severe pre-eclampsia?

A

BP over 160 systolic or 110 diastolic
Proteinuria over 5g or +++ on dipstick
Oliguria under 400ml in 24 hours
CNS signs
Pulmonary oedema
Epigastric/RUQ pain
Impaired LFTs
Thrombocytopenia
IUGR
Oligohydramnios

511
Q

Definitive cure for pre-eclampsia?

A

Delivery of placenta

512
Q

Low birth weight? Very low birth weight? Extremely low birth weight?

A

Low= under 2500g
Very low= under 1500g
Extremely low= under 1000g

513
Q

Primary prevention methods for preventing preterm birth?

A

Smoking cessation, STI prevention, prevent multiple pregnancy (IVF caution), variable work schedules, physical and sexual activity advice, cervical assessment at 20-26 weeks

514
Q

Secondary prevention methods for preventing preterm birth?

A

Transvaginal cervical ultrasound, qualitative foetal fibronectin test
Screen high risk asymptomatic women
Manage women with threatened preterm labour with a cervix under 3cm dilated- administer progesterone (pessary), cervical cerclage can be used

515
Q

How can you manage a woman with threatened preterm birth?

A

Intravaginal progesterone first line
Cervical cerclage can be used

516
Q

Tertiary prevention methods for preventing preterm birth?

A

Prompt diagnosis, tocolysis and antibiotics, corticosteroids

517
Q

What is foetal fibronectin? significance of it?

A

Extracellular matrix protein found in choriodecidual interface
Abnormal finding in cervicovaginal fluid after 20 weeks so may indicate disruption of attachment of membranes to decidua
Reappears close to term as labour approaches

518
Q

What test to look for foetal fibronectin/ FDC-6? downfalls?

A

ELISA
NB/ false positives eg cervical manipulation, sexual intercourse, lubricants, bleeding

519
Q

How far away must placenta be from internal cervical os to be considered normal?

A

At least 20mm

520
Q

General management for any worrying APH?

A

ABCDE
2 14/16 G cannulas
IV fluids (crystalloid)
Cross match 6 units
Inform senior colleagues and paediatrics
Examination (avoid digital exam)
Foetal monitoring +/- delivery
Steroids if under 34 weeks

521
Q

Complications of antepartum haemorrhage?

A

Premature labour/delivery, blood transfusion, acute tubular necrosis (+/- renal failure), DIC, PPH, ITU admission, ARDS (secondary to transfusion), foetal morbidity and mortality

522
Q

Uterotonic options?

A

Oxytocine, ergometrine, carboprost, misoprostol, tranexamic acid

523
Q

Sepsis 6?

A

Give three, take three
oxygen, IV abx, IV fluids
Blood cultures, bloods (hb/lactate/glucose), measure hourly urine output

524
Q

Describe the follicular phase of the menstrual cycle?

A

Low oestrogen and progesterone
Increasing levels of FSH
Developing follicles release oestrogen
This inhibits FSH and leads to one dominant follicle
Oestrogen levels rise high enough to induce positive feedback on pituitary (not negative)
LH surge= ovulation

525
Q

Describe the luteal phase of the menstrual cycle?

A

Follicle forms corpus luteum which secretes progesterone
Progesterone peaks 7 days after ovulation and unless maintained by the pregnancy, corpus luteum regresses to corpus albicans
Falling progesterone induces menstruation

526
Q

When does progesterone level peak in menstrual cycle?

A

7 days after ovulation

eg day 21 in 28 day cycle
eg day 28 in 35 day cycle

527
Q

How many days from ovulation to menstruation?

A

14 days

528
Q

What maintains the corpus luteum in pregnancy?

A

HCG secreted by synctiotrophoblast (similar to FSH and LH)
Continues to secrete progesterone until the placenta takes over at about 12 weeks

529
Q

How does the COCP work?

A

provides a constant level of oestrogen and progestogen, causes negative feedback on FSH and LH
This prevents development of follicles and stops the LH surge so no ovulation!

530
Q

In fertility investigations, when to check baseline FSH and LH?

A

Day 2-5

531
Q

What happens in the menstrual phase of the menstrual cycle?

A

Falling levels of progesterone cause shedding of the endometrium; spasm of spiral arterioles, ischaemic necrosis and generalised inflammation

532
Q

What happens in the proliferative phase of the menstrual cycle?

A

Endometrium grows under the influence of oestrogen. Early development of glands and spiral arterioles

533
Q

What happens in the secretory phase of the menstrual cycle?

A

After ovulation, progesterone dominates
Development of complex glands, increase in spiral arterioles, endometrial cells produce and store glycogen
Endometrium stops growing so much but prepares for implantation

534
Q

Why do obese people produce more oestrogen?

A

Increased aromatase

535
Q

How do progestogen contraceptives work?

A

Maintain the thin uterine lining and inhibit action of oestrogen- stops menstruation by avoiding the drop in progesterone before menstruation

536
Q

What is cervical motion tenderness or cervical excitation seen in?

A

PID and ectopic pregnancy

537
Q

What is pelvic congestion syndrome?

A

Incompetence of pelvic vein valves, typically occurring after pregnancy
Causes constant dull lower abdo ache which is worse after standing/exercise

538
Q

How to investigate pelvic congestion syndrome? How to manage?

A

Transvaginal duplex USS or MRI venogram
Mx= analgesia, or non invasive transcatheter vein embolisation

539
Q

How common is failure to conceive after 1 year?

A

15-25% of couples will not have conceived after 1 year.

540
Q

Common causes of infertility?

A

Male 30%
Ovulatory 25%
Tubal 20%
Uterine/peritoneal 10%
unexplained - 25%

541
Q

Criteria for early referral regarding infertility?

A
  • female age >35
  • known or suspected problem
542
Q

Criteria for early referral regarding infertility?

A
  • female age >35
  • known or suspected problem e.g. menstrual disorder
  • previous abdo/pelvic surgery
  • previous PID/STD
543
Q

What preconception advice is given to couples trying to conceive?

A
  • Intercourse – 2-3 x week
  • Folic acid – 0.4mg (5mg high risk)
  • Smear
  • Rubella
  • Smoking – cessation services
  • Pre-existing medical conditions
  • Drug history (prescribed / recreational)
  • Environmental / occupational exposure
  • Alcohol (women none
  • Weight (BMI 19 – 30)
544
Q

Primary care investigations for infertility?

A
  • Hormone profile (D2 FSH, D21 Prog)
  • TFT, Prolactin if indicated
  • Rubella
  • Smear
  • Swabs
  • Semen analysis
545
Q

Investigations for female infertility?

A
  • mid-luteal progesterone (ovulation)
  • ovarian reserve testing (ovulation)
  • Tubal/uterus patency
546
Q

Mid-luteal progesterone values? (anovular, ovular)

A

<16 anov

16-30 equivocal

>30 ovular

547
Q

How is tubal/uterine patency investigated in infertility?

A

Hysterosalpingogram (HSG)

Laparoscopy + dye = when pathology suspected e.g. PID, pain, previous surgery

548
Q

Grouping of ovulation disorders? (WHO groups 1-3, other)

A

Group 1: Hypogonadotropic (10%)

  • ↓hypoFSH/LH, ↓hypoE2
  • hypothalamic-pituitary problem: decreased secretion or pituitary unresponsiveness
  • ammenorrhea (stress, weight loss, exercise), Sheehan’s syndrome, tumours

Group 2: Normogonadotrophic (85%)

  • normal FSH/LH, normal E2
  • pituitary-ovaries problem
  • PCOS, hyperprolactinaemic ammenorrhea (prolactin inhibits gonadotropins)

Group 3: Hypergonadotrophic (5%)

  • ↑hyperFSH/LH, ↓hypoE2
  • premature ovarian failure

Other: thyroid, adrenal

549
Q

Treatment of ovulation disorders (WHO groups 1-3)?

A

Group 1 (hypogonadotropic): FSH+LH, GnRH pump, normalise weight

Group 2 (normogonadotropic): Induce ovulation with clomifene

Groupo 3: (hypergonadotropic): Donor egg

550
Q

Infertility treatment in group 2 ovulation disorders/PCOS?

A
  1. Normalise weight
  2. Clomifene/tamoxifen):
  • Up to 6 cycles
  • Stop after 12 mo (increased ovarian cancer risk)
  • Monitor (Progesterone & USS)
  • Inform of multiple preg rate (6-8%)

3.Metformin may help if clomifene resistant

Further tx:

ovarian drilling

GnRh ovulation induction

551
Q

Causes of tubal disease infertility?

A
  • Infections: Chlamydia, Gonorrhoea
  • Endometriosis
  • Surgical:Adhesions, Sterilisation
552
Q

Treatment for endometriosis infertility?

A
  • Laparoscopic ablation
  • Laparoscopic cystectomy for endometriomas
553
Q

Treatment of unexplained infertility?

A

IVF

554
Q

Risks of IVF?

A
  • Multiple Pregnancy
  • Miscarriage
  • Ectopic
  • Fetal abnormality
555
Q

What should happen to baby’s heart during and after contractions?

A
  • Decrease during contraction
  • Increased after contraction
  • If no increase after contraction, problem
556
Q

How common is stillbirth in the UK?

A
  • 5/1000 live births
  • one of the highest rates in the developed world
557
Q

Indications for a high risk pregnancy (obstetrician lead rather than midwifery lead)?

A
  • Underlying medical conditions: Hypertension, Diabetes, Epilepsy, Rheumatoid arthritis, Asthma, most medical conditions
  • Issues with woman: high/low BMI, smoking/alcohol/drugs, old/young
  • Complications in previous pregnancy: c-section, traumatic delivery, 3rd/4th degree tear, pre-eclampsia, preterm birth
  • Complications in current pregnancy: multiple pregnancy, breech presentation, pre-eclampsia, gestational diabetes
558
Q

If a pregnancy is classified as high risk, what does this mean for fetal monitoring?

A

High risk pregnancies need continuous monitoring with CTG.

(Low risk pregnancies will have intermittent auscultation with pinnard stethoscope or handheld doppler.)

559
Q

Normal range for CTGs?

  • baseline
  • variability
  • accels/decels

Conditions for a CTG to be classed as normal?

A
  • baseline: 110-160bpm
  • variability: >5bpm
  • accels: present
  • decels: early
  • all 4 features need to be within range for CTG to be reassuring
  • CTG can be suspicious (1 non-reassuring feature) or pathological (2 non-reassuring features/1 abnormal feature)
560
Q

Tools available for continuous monitoring of fetal heart rate?

A
  • CTG (doppler ultrasound)
  • Fetal scalp electrocardiogram/ecg - used only in labour
  • Abdominal fetal ECG - not widely available
561
Q

What is cardiotocography (CTG?)

A

Doppler ultrasound used to measure fetal heart rate (FHR).

562
Q

Frothy discharge indicates?

A

Trichomonas vaginalis

563
Q

Strawberry cervix indicates?

A

Trichomonas vaginalis

564
Q

Mirabegron:

  • use
  • mechanism
  • contraindication
A
  • Overactive bladder if anticholinergics not suitable
  • relaxes sm and increases bladder capacity
  • uncontrolled bp
565
Q

What causes the symptoms seen in menopause?

A

Decreasing oestrogen levels lead to:

Short term

  • vasomotor: hot flushes, night sweats
  • general: mood change, irritability, loss of memory/concentration, headaches, dry/itchy skin

Medium term

  • urogenital atrophy: dyspareunia, reucurrent UTIs, PMB

Long term

osteoporosis

CVD and dementia if early menopause

566
Q

How does the risk of breast cancer change when on HRT containing

  • oestrogen
  • oestrogen+progesterone?
A

Oestrogen: little or no change

Oestrogen + Progesterone: increased risk

depends on duration of treatment and decreases once treatment stops

567
Q

A woman who is on HRT for menopausal symptoms has just been diagnosed with breast cancer. What must you do?

A

Discontinue HRT immediately.

568
Q

How do oral and transdermal HRT affect risk of VTE?

A

oral HRT: significantly increased

transdermal: no change

569
Q

How do oral and transdermal HRT affect risk of stroke?

A

oral: slightly increased
transdermal: no change

570
Q

How does HRT affect risk of CVD?

A
  • HRT does not increase cardiovascular risk when started in women < 60 years
  • The presence of cardiovascular risk factors is not a CI to HRT as long as they are optimally managed
571
Q

For a woman with a uterus you have to give oestrogen+progesterone, but for a woman with no uterus you can give unopposed oestrogen. Why?

A

Oestrogen causes proliferation of endometrium. In a woman with a uterus, unopposed oestrogen could lead to endometrial hyperplasia>>neoplasia>>cancer, so we give progesterone to counteract this. In a woman with no uterus;no endometrium, there is no risk of this so can give unopposed oestrogen.

572
Q

HRT regime options?

A

Oestrogen: oral, gel, patch, vaginal lubricant (for atrophy symptoms)

+

Progesterone: continuous (Mirena coil, tibolone) or sequential

573
Q

What are the pros and cons of taking continuous combined HRT vs sequential HRT?

A

Continuous combined: 1/50 risk of breast cancer but no bleeds

Sequential: 1/70 risk but bleeds

574
Q

When should transdermal oestrogen be prescribed for HRT instead of oral?

A
  • Gastric upset eg Crohns
  • Increased risk of VTE including
  • CVD risk factors: hypertension, BMI>30
  • Need for steady absorption eg migraine/epilepsy
  • Concomitant hepatic enzyme-inducing drug treatment (for example carbamazepine).
  • Lactose sensitivity
  • Patient choice
575
Q

How long can the Mirena IUS be used for in

  • contraception
  • HRT?
A
  • Contraception: 5 yrs
  • HRT: 4 yrs
576
Q

HRT contraindications and cautions?

A

Cautions

  • Current, past, or suspected breast cancer
  • Undiagnosed vaginal bleeding
  • VTE
  • arterial thromboembolic disease e.g. angina or myocardial infarct
  • Active liver disease with abnormal liver function tests.
  • Pregnancy.
  • Thrombophilic disorder
  • caution
    • Diabetes mellitus (increased risk of heart disease).
    • Factors predisposing to venous thromboembolism.
    • History of endometrial hyperplasia.
    • Migraine and migraine-like headaches.
577
Q

Non-hormal HRT options?

A

Alpha adrenergic receptor agonist–Clonidine

SSRI–Fluoxetine–Paroxetine–Citalopram–Sertraline–

SSRI-SNRI–Venlafaxine

Anti-epileptics–Gabapentin

578
Q

Which non-hormonal HRT options are contraindicated in women on tamoxifen for breast cancer?

A

SSRIs: fluoxetine and paroxetine

579
Q

What are the long-term complications of early menopause and what does this mean for management?

A

Early osteoporosis

Early CVD

Early cognitive decline (dementia)

This means women with early menopause should be on HRT.

580
Q

Do women who have undergone early menopause need to be on contraception?

A

Yes

Fertile for 2 years if menopause <50 years

Fertile for 1 year of menopause >50 years

Phase 3A 2021 (7 decks)

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