Obs + Gynae Flashcards

1
Q

How does renal plasma flow change in pregnancy?

A

Increases
Increases during early trimesters, decreases towards end of third trimester

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2
Q

How does total plasma volume change in pregnancy?

A

Increases: 30-50%

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3
Q

Changes in heart in pregnancy?

A

Increased cardiac output
Increased stroke volume
Increased heart rate

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4
Q

Changes in oncotic/osmotic pressure in pregnancy

A

Decreased serum albumin concentration
Decreased serum colloid osmotic pressure

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5
Q

Changes in clotting system in pregnancy

A

Increased coagulation factors
Increased fibrinogen

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6
Q

Changes in kidneys in pregnancy

A

Increased renal blood flow
Increased GFR

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7
Q

Changes in lungs in pregnancy

A

Increased tidal volume
Increased minute ventilation

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8
Q

Changes in GI system in pregnancy

A

Nausea + vomiting
Delayed gastric emptying
Prolonged small bowel transit time
Gastrointestinal reflux

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9
Q

Normal physiological changes seen on blood tests in pregnancy

A

Slight anaemia
Slightly lowered platelets
Increased ALP
Decreased albumin, AST + ALT
Increased GFR
–> decreased Urea + Creatinine –> if Ur + Cr are even slightly raised, this can indicate serious renal disease

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10
Q

Causes of antepartum haemorrhage

A

Placental abruption
Placenta praevia
Vasa praevia
Uterine rupture
Unexplained

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11
Q

What is vasa praevia

A

Foetal vessels run in membranes below the presenting foetal part, unsupported by placental tissue or umbilical cord

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12
Q

How does vasa praevia present?

A

PV bleeding (dark red)
After rupture of foetal membranes
Shock consistent with external loss
Painless bleeding
Rapid foetal distress

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13
Q

Risk factors for vasa praevia

A

Low-lying placenta
Multiple pregnancy
IVF pregnancy
Bilobed (succenturiate lobed) placentas

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14
Q

Management of vasa praevia

A

ABCDE assessment + resuscitation
Caesarean section
Monitor during pregnancy
Elective caesarean at 34-36 weeks

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15
Q

What is placenta praevia?

A

When the placenta is inserted wholly, or in part, into the lower segment of the uterus

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16
Q

What is major placenta praevia?

A

Grade III or IV
Placenta lies over the cervical os

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17
Q

Why is major placenta praevia concerning?

A

Cervical effacement and dilatation would result in catastrophic bleeding

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18
Q

What is minor placenta praevia?

A

Grade I or II
Placenta lies in lower segment, close to, or encroaching on the cervical OS

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19
Q

Risk factor for placenta praevia

A

Previous Caesarean section
Increased age
Maternal smoking
IVF

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20
Q

Presentation of placenta praevia haemorrhage

A

Painless, red PV bleeding
Profuse bleeding (shock consistent with external loss)
Often smaller previous APHs
Foetus may have abnormal lie

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21
Q

Management of placenta praevia

A

ABCDE assessment + resuscitation
Caesarean section

Monitor during pregnancy
Elective caesarean at 38 weeks

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22
Q

Presentation of placental abruption

A

Painful PV bleeding
PV loss does not correlate with shock (some women have no external loss)
Uterus = tender + firm (woody hard)
Pain is constant, with exacerbations
Foetal distress
May present in labour

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23
Q

Risk factor for placental abruption

A

ABRUPTION
Abruption previously
Blood pressure e.g. hypertension or pre-eclampsia
Ruptured membranes (premature or prolonged)
Uterine injury
Polyhydramnios
Twins/multiple gestation
Infection in the uterus
Older age (>35)
Narcotic use (cocaine, amphetamines, and smoking)

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24
Q

Placenta accreta

A

Placental villi are attached to the myometrium

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25
Q

Placenta increta

A

Villi invaded into >50% of the myometrium

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26
Q

Placenta percreta

A

Villi pass through whole myometrium up to the serosa
May involve other viscera e.g. bladder or bowel

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27
Q

Risk factors for abnormal placentation

A

Uterine surgery e.g. CS or myomectomy
Repeated surgical termination of pregnancy
IVF
Maternal age >35

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28
Q

Management of placenta accreta post delivery

A

Heavy bleeding:
- Blood replacement
- Balloon tamponade e.g. Rusch
- Hysterectomy
Minimal bleeding:
- Leave placenta in situ + monitor

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29
Q

Threatened miscarriage

A

Bleeding +/- abdominal pain
Closed cervix
Foetus alive
Before 24 weeks (usually 6-9 weeks)

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30
Q

Management of threatened misscarriage

A

Anti-D if >12 weeks or heavy bleeding, or pain on RhD-ve women
Sonography

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31
Q

Missed miscarriage

A

Cervical os closed
Foetus no longer alive
No symptoms have occurred - may have some light vaginal bleeding
Pregnancy symptoms may decrease

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32
Q

USS findings of missed miscarriage

A

Foetal pole >7mm
No foetal heart activity
Mean gestation sac diameter >25mm with no foetal pole or yolk sac

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33
Q

Management of missed miscarriage

A

Expectant/medical/surgical

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34
Q

Inevitable miscarriage

A

Bleeding +/- pain
Open cervical os
May have foetus with possible heartbeat

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35
Q

Management of inevitable miscarriage

A

Expectant/medical/surgical

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36
Q

Use of Anti-D in miscarriages

A

Given if >12 weeks, or heavy bleeding or pain in Rh-D -ve women

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37
Q

Presentation of incomplete miscarriage

A

Bleeding +/- pain with passage of large clots or tissue
Possible open cervical os - products of conception may be seen in dilated cervical os
Not all products of conception have been expelled

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38
Q

Presentation of complete miscarriage

A

Bleeding and pain cease
Closed cervix
USS: empty uterus, endometrial thickness <15 mm

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39
Q

Expectant management of miscarriage

A

Used if not bleeding heavily
Very effective in incomplete miscarriages
Less effective in women with intact sac
Repeat TVS at 2 weeks to ensure complete miscarriage
Surgical evacuation offered at later date

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40
Q

Medical management of miscarriage

A

Prostaglandin analogues (misoprostol) often given vaginally

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41
Q

How long might bleeding continue after medical management of miscarriage?

A

3 weeks after medical uterine evacuation

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42
Q

Surgical management of miscarriage

A

Evacuation of retained products of conception if there is excessive or persistent bleeding, or surgical management requested
Suction curettage used

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43
Q

Complications of surgical management of miscarriage

A

Infection
Haemorrhage
Uterine perforation
Retained products
Intrauterine adhesions
Cervical tears
Intraabdominal trauma

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44
Q

How can uterine and cervical trauma caused by surgical management of miscarriage be reduced?

A

Giving prostaglandin (misopristol or gemeprost) before the procedure

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45
Q

What is the 1st stage of labour divided into?

A

Latent phase
Active phase

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46
Q

How is the latent phase of labour defined?

A

Period taken for cervix to completely efface and dilate up to 3cm

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47
Q

How is the active phase of labour defined?

A

3cm-10cm full dilatation

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48
Q

Expected rate of cervical dilatation in the active phase

A

1cm/hour

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49
Q

When would failure to progress be considered in active phase of stage 1 of labour

A

<2cm dilatation in 2hour
Slowing in progress in parous women

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50
Q

Causes of poor progress in 1st stage of labour

A

Power - inefficient uterine activity (commonest)
Passenger - malpositions, malpresentation, or large baby
Passage - inadequate pelvis
Combination

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51
Q

Management of poor progress in 1st stage of labour

A

Membrane sweep
Prostaglandin pessary (as inpatient)
Amniotomy (artificial rupture of membranes) and reassess in 2 hours
Amniotomy + oxytocin infusion and reassess in2 hours (especially in nulliparous women)
Lower segment CS (if foetal distress)

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52
Q

What is Stage 2 of labour?

A

From full dilatation to delivery of the foetus

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53
Q

How long does Stage 2 normally last?

A

1 hour of active pushing
Should last no longer than 3h in nulliparous women, 2h in multiparous women

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54
Q

Causes of delay in Stage 2 of labour

A

Brow presentation
Face presentation
Compound/shoulder presentation
Transverse lie
Occiput posterior/Occiput Transverse position
Disproportion

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55
Q

Management of delay in Stage 2 of labour

A

Instrumental delivery e.g. ventouse, forceps
Surgical delivery

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56
Q

Risk factors for ovarian cancer

A

Nulliparity
Early menarche and/or late menopause (increased ovulations)
BRCA gene mutations
HNPCC (Lynch II syndrome)
Age
Obesity
Smoking
Recurrent use of clomifene

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57
Q

Factors that decrease the risk of ovarian cancer

A

COCP
Pregnancy
Breastfeeding

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58
Q

Presentation of ovarian cancer

A

Vague, common symptoms
Abdominal discomfort/distension (bloating, but persistent)
Early satiety
Loss of appetite
Pelvic pain
Increased girth/ascites
Urinary symptoms
Change in bowel habits
Abnormal vaginal bleeding
Detection of pelvic mass

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59
Q

Blood tests for ovarian cancer

A

FBC, U+E, LFTs (albumin)
Tumour markers

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60
Q

Examination findings for ovarian cancer

A

Pelvic/abdominal mass
Ascites
Omental mass (common site for metastasis) –> ommental cake
Pleural effusion
Supraclavicular lymph nodes

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61
Q

Tumour markers in ovarian cancer

A
  • CA125 increased in 80% epithelial cancers
  • CEA (carcinoembryonic antigen): raised in CRC, normal in ovarian cancer
  • CA19.9: may be raised in mucinous tumours (also pancreas + breast)
  • Others (for rarer tumours): AFP, hCG, LDH, inhibin, oestradiol
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62
Q

Imaging for ovarian cancer

A

Abdominal/pelvic USS
CXR
CT abdomen/pelvis

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63
Q

Potential findings on USS for ovarian cancer

A

Presence of pelvic mass
Ascites

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64
Q

Potential findings on CXR for ovarian cancer

A

Pleural effusion or lung metastases (for staging and properative assessment)

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65
Q

Potential findings on CT abdo/pelvis for ovarian cancer

A

Omental caking
Peritoneal implants
Liver metastases
Para-aortic lymph nodes

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66
Q

Stage I of ovarian cancer

A

Limited to ovaries
Ia = one ovary
Ib = two ovaries
Ic =ruptured capsule, tumour on ovarian surface, or positive peritoneal washings/ascites

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67
Q

Stage II of ovarian cancer

A

Limited to pelvis
IIa = uterus or tubes
IIb = other pelvic structures
IIc = positive peritoneal washing/ascites

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68
Q

Stage III of ovarian cancer

A

Limited to abdomen (including regional lymph node mets)
IIIa =- microscopic metastases
IIIb = macroscopic mets <2cm
IIIc = macroscopic mets >2cm

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69
Q

Stage IV of ovarian cancer

A

Distant mets outside abdominal cavity

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70
Q

5 types of epithelial cell ovarian cancers

A

Serous tumours (most common)
Endometroid carcinomas
Clear cell tumours
Mucinous tumours
Undifferentiated tumours

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71
Q

What might cause hip or groin pain with an ovarian mass?

A

Compression of the obturator nerve

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72
Q

What three factors does the risk of malignnacy index (RMI) take into account for ovarian masses?

A

Menopausal status
Ultrasound findings
CA125 level

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73
Q

Causes of raised CA125

A

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy
Ovarian cancer, breast cancer, metastatic lung cancer, endometrial cancer (not vulval)
Ascites
Menstruation
Ovarian torsion

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74
Q

Surgical management of ovarian cancer

A

Total abdominal hysterectomy
Bilateral salpingo-oophrectomy
Infracolic omentectomy
Lymph node sampling (pelvic + para-aortic)
Peritoneal biopsies
Pelvic washings
Sampling of ascites

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75
Q

Medical management of ovarian cancer

A

Adjunct to surgical management
Chemotherapy: carboplatin + paclitaxel
Monitor response using CA-125 levels
Intraperitoneal chemotherapy

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76
Q

What is stress incontinence

A

Loss of urine associated with a rise in intrabdominal pressure e.g. coughing or sneezing
Due to weakness of pelvic floor and sphincter muscles

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77
Q

Risk factors for stress incontinence

A

Increasing age
Traumatic vaginal delivery
Obesity
Previous pelvic surgery

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78
Q

What is urge inctontinence?

A

Caused by overactivity of the detrusor muscle of the bladder (overactive bladder)

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79
Q

What is mixed incontinence?

A

A combination of urge incontinence and stress incontinence

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80
Q

Risk factors for urge incontinence

A

Increased age
Obesity
Smoking
Family history
Diabetes mellitus

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81
Q

When might overflow incontinence occur?

A

When there is chronic urinary retention due to an obstruction of outflow of urine
Occurs without the urge to pass urine
More common in men

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82
Q

Causes of overflow incontinence in women

A

Anticholinergic medications
Fibroids
Pelvic tumours
Neuro conditions e.g. MS, diabetic neuropathy, spinal cord injuries

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83
Q

Modifiable lifestyle factors that may contribute to incontinence symptoms

A

Caffeine consumption
Alcohol consumption
Medications
BMI

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84
Q

Modified Oxford grading system for strength of pelvic muscle contractions on bimanual examination

A

0 - no contraction
1: faint contraction
2: weak contraction
3: moderate contraction with some resistance
4: good contraction with resistance
5: strong contraction, a firm squeeze, and drawing inwards

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85
Q

Investigations for incontinence

A

Bladder diary - fluid intake, urination and incontinence
Urine dipstick testing - rule out UTI or DM
Post-void residual bladder volume
Urodynamic testing (urge incontince if not responding or other features)

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86
Q

Management of stress incontinence

A

Avoidance of caffeine, diuretics and overfilling bladeder
Avoid excessive or restricted fluid intake
Weight loss
Supervised pelvic floor exercises (3 months)
Surgery
Duloxetine (where surgery is less preferred)

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87
Q

Surgical management options for stress incontinence

A

Tension-free vaginal tape
Autologous sling procedures (uses fascia instead of tape)
Colposuspension
Intramural urethral bulking

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88
Q

Management of urge incontinence

A

Bladder retraining for at least 6 weeks (first line)
Anticholinergic medication e.g. oxybutynin, tolterodine, solifenacin
Mirabegron as alternative medication
Invasive procedures

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89
Q

Anticholinergic side effects

A

Dry mouth
Dry eyes
Urinary retention
Constipation
Postural hypotension
Cognitive decline, memory problems, and worsening of dementia

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90
Q

When is mirabegron contraindicated for an overactive bladder/incontinence

A

In uncontrolled hypertension

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91
Q

Invasive management options for urge incontinence

A

Botox bladder injections
Percutaneous sacral nerve stimulation
Augmentation cystoplasty
Urinary diversion

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92
Q

What is red degeneration of a fibroid

A

Ischaemia, infarction and necrosis of fibroid due to disrupted blood supply - common in 2nd and 3rd trimester of pregnancy due to fibroid rapidly outgrowing blood supply, uterus changing shape and therefore arteries kinking

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93
Q

Classical patient of red degeneration of fibroid

A

Pregnant women - often 2nd and 3rd trimester
History of fibroids - or history of heavy periods and difficulty concieving etc
Severe abdominal pain and low-grade fever, tachycardia, vomiting

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94
Q

Management of red degeneration of fibroid

A

Supportive
Rest, fluids, analgesia

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95
Q

Commonest causes of PID

A

Neisseria gonorrhoeae –> tends to produce more severe PID
Chlamydia trachomatis
Mycoplasma genitalium

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96
Q

Risk factors for PID

A

No barrier contraception
Multiple sexual partners
Younger age
Existing STIs
Previous PID
Intrauterine device

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97
Q

Symptoms of PID

A

Pelvic or lower abdominal pain
Abnormal vaginal discharge
Abnormal bleeding e.g. intermenstrual or postcoital
Pain during sex (dyspareunia)
Fever
Dysuria

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98
Q

Examination findings in PID

A

Pelvic tenderness
Cervical excitation (motion tenderness)
Inflamed cervix
Purulent discharge

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99
Q

Investigations in PID

A

NAAT swabs - gonorrhoea, chlamydia, mycoplasma genitalium if available
HIV + syphylis test
High vaginal swab - bacterial vaginosis, candidiasis, trichomoniasis
Look for pus cells on swab from vagina or endocervix, under microscope (absence useful in excluding)
Pregnancy test - rule out ectopic
Inflammatory markers - raised

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100
Q

Management of PID

A

Referral to GUM
Contact tracing
Start antibiotics before swab results obtained: doxycycline, metronidazole, IM ceftriaxone
Leave in recently inserted coil. If no response within 72 hours, remove coil + prescribe any other necessary emergency contraceptives

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101
Q

Complications of PID

A

Sepsis
Abscess
Infertility
Chronic pevlis pain
Ectopic pregnany
Fitz-Hugh-Curtis syndrome

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102
Q

What is Fitz-Hugh-Curtis syndrome

A

Complication of PID
Caused by inflammation and infection of the liver capsule –> adhesions between liver and peritoneum
RUQ pain (can be referred to right shoulder)
Adhesiolysis required

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103
Q

USS measurements for assessing foetal size

A

Estimated foetal weight
Foetal abdominal circumference

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104
Q

Antibiotic usage in UTI in pregnancy

A

Nitrofurantoin (avoid in third trimester)
Amoxicillin
Cefalexin

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105
Q

Nitrofurantoin in pregnancy

A

Avoided in 3rd trimester due to risk of haemolytic anaemia

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106
Q

Trimethoprim in pregnancy

A

Avoided in 1st trimester
Folate antagonist –> neural tube defects

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107
Q

Sulfonamides in pregnancy

A

Avoided in 3rd trimester as are associated with kernicterus (brain damage due to high levels of billirubin)

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108
Q

Tetracyclines in pregnancy

A

Avoided as cause permanent staining of baby’s teeth, and problems with skeletal development

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109
Q

Intramural fibroids

A

Within myometrium
As they grow, they change the shape and distort the uterus

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110
Q

Subserosal fibroids

A

Just below outer layer of uterus
Grow outwards and can become very large, filling abdominal cavity

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111
Q

Submucosal fibroids

A

Just below endometrium
Can be resected hysteropically

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112
Q

Presentation of fibroids

A

Often asymptomatic
Menorrhagia
Prolonged menstruation (>7 days)
Abdominal pain, worse during menstruation
Bloating/feeling full in abdomen
Urinary or bowel symptoms due to pelvic pressure or fullness
Deep dyspareunia
Reduced fertility
Palpable pelvic mass, or enlarged firm non-tender uterus

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113
Q

Investigations of fibroids

A

Hyteroscopy for submucosal fibroids with heavy menstrual bleeding
Pelvic ultrasound for larger fibroids
MRI scanning may be considered before surgical options

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114
Q

Management of fibroids <3 cm

A

Same as for heavy menstrual bleeding
Mirena coil
Symptomatic management - NSAIDS + tranexamic acid
COCP
Cyclical oral progestogens

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115
Q

Management of heavy menstrual bleeding

A

If no identigied pathology, fibroids <3cm diameter or suspected/diagnosed adenomyosis –>
1st line = LNG-IUS
If declines or not suitable:
- Non-hormonal = tranexamic acid, NSAIDs
- Hormonal = COCP, cyclical oral progestogens

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116
Q

Surgical management for smaller fibroids with HMB

A

Endometrial ablation
Resection of submucosal fibroids during hysteroscopy
Hysterectomy

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117
Q

Management of fibroids >3cm

A

Symptomatic - NSAIDs, tranexamic acid
Mirena coil - depends on size + shape
COCP
Cyclical oral progestogens

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118
Q

Surgical management of larger fibroids

A

Uterine artery embolisation
Myomectomy (preserves ferility)
Hysterectomy

GnRH agonists prior to surgery to shrink fibroid

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119
Q

Symptoms of endometriosis

A

Cyclical abdominal or pelvic pain
Deep dyspareunia
Dysmennorhoea
Infertility/subfertility
Cyclical bleeding from other sites
May also suffer from continuous pain e.g. with adhesions
Urinary symptoms
Bowel symptoms

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120
Q

Possible examination findings in endometriosis

A

Endometrial tissue visible in vagina on speculum, especially in posterior fornix
Fixed cervix on bimanual
Tenderness in the vagina, cervix, and adnexa

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121
Q

Diagnosis of endometriosis

A

Gold standard = laparoscopic surgery + biopsy
Pelvic USS may reveal large endometriomas and chocolate cysts, but often unremarkeable

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122
Q

Management of endometriosis

A

Analgesia e.g. NSAIDs +/- paracetamol
Hormonal management: COCP, POP, Depo-Provera, Nexplanon implant, Mirena coil, GnRH agonists
Surgical management: laparoscopic surgery to excise or ablate tissue, and adhesiolysis. Surgery is only way to improve fertility
Final solution = hysterectomy + bilateral salpingo-oophrectomy.

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123
Q

Risk factors for ectopic pregnancy

A

Previous ectopic
Previous PID
Previous surgery to fallopian tubes
IUDs
Older age (>35)
Smoking
Age <18 at first sexual intercourse
Black
IVF

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124
Q

Presentation of ectopic pregnancy

A

Typically 6-8 weeks gestation
Missed period
Constant lower abdominal pain (LIF or RIF)
Vaginal bleeding
Lower abdominal or pelvic tenderness
Cervical motion tenderness

Dizziness or syncope
Shoulder tip pain (peritonitis)

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125
Q

USS findings for ectopic pregnancy

A

Transvaginal USS
Gestational sac containing yolk sac or foetal pole seen in a fallopian tube
Sometimes non-sepcific mass in tube
Mass containing empty gestational sac = blob/bagel/tubal ring sign
Mass moves separately to ovary, but looks like corpus luteum
Empty uterus/fluid in uterus (pseudogestational sac)

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126
Q

Management of pregnancy of unknown location

A

Serum hCG tracked over time - baseline + repeated at 48 hours to monitor (should double in normal pregnancy)
If hCG rises >63% –> repeat USS in 1-2 weeks to confirm intrauterine pregnancy
If rise <63% –> likely ectopic pregnancy
Fall >50% –> likely miscarriage –> urinary pregnancy test in 2 weeks to confirm completeness

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127
Q

Management of ectopic pregnancy

A

Expectant management
Medical management e.g. methotrexate
Surgical management - salpingectomy or salpingotomy (salpingotomy if risk factors for infertility e.g. csontralateral tube damage)

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128
Q

Criteria for expectant management of ectopic pregnancy

A

Follow-up must be possible
Unruptured ectopic
Adnexal mass <35 mm
No visible heartbeat
No significant pain
hCG >1000IU/L, <1500IU/L

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129
Q

Criteria for methotrexate management of ectopic pregnancy

A

Follow-up must be possible
Unruptured ectopic
Adnexal mass <35 mm
No visible heartbeat
No significant pain
hCG <1500 IU/L
Confirmed absence of intrauterine pregnancy on USS

Advised not to get pregnant for 3 months after treatment

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130
Q

Features for diagnosis of PCOS

A

Two of:
- Anovulation/oligo-ovulation
- Hyperandrogenism
- Polycystic ovaries on USS (string of pearls appearance)/increase ovarian volume

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131
Q

Symptoms of ovarian cysts (uncomplicated)

A

Pelvic pain
Bloating
Fullness in abdomen
Palpable pelvic mass

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132
Q

Follicular cysts

A

Commonest type of ovarian cyst
Developing follicle that fails to rupture –> cyst persists
Tend to disappear after a few menstrual cycles
Thin walls + no internal structures

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133
Q

Corpus luteum cysts

A

Occurs when corpus luteum fails to break down –> fills with fluid
Often seen in early pregnancy
May cause pelvic discomfort, pain, or delayed menstruation

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134
Q

Who does not require further investigation for ovarian cyst

A

Premenopausal women
Simple cyst <5cm on ultrasound

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135
Q

Women under 40 years with complex ovarian mass require what tumour marks for possible germ cell tumour

A

Lactate dehydrogenase (LDH)
Alpha-fetoprotein
Human chorionic gonadotropin

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136
Q

Management of simple ovarian cysts <5cm in premenopausal women

A

Tend to resolve within 3 cycles
No follow-up scan required

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137
Q

Management of simple ovarian cysts 5-7cm in premenopausal women

A

Routine referral to gynaecology
Yearly ultrasound monitoring

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138
Q

Management of simple ovarian cysts >7cm in premenopausal women

A

Consider MRI or surgical evaluation as hard to characterise with USS

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139
Q

Management of ovarian cysts in postmenopausal women

A

Correlate with CA125 result
Refer to gynaecologist (2 week wait if raised CA125)
Simple cysts <5cm –> monitored with 4-6months USS
Surgical intervention if required

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140
Q

Meig’s syndrome

A

Ovarian fibroma (benign ovarian tumour)
Pleural effusion
Ascites
Removal of tumour results in resolution of effusion + ascites
presents in older women

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141
Q

When is ovarian torsion more likely to occur

A

Ovarian mass >5cm e.g. cyst or tumour (more likely with benign tumours)
During pregnancy
In younger girls before menarche due to longer infundibulopelvic ligaments

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142
Q

Presentation of ovarian torsion

A

Pelvic pain:
- Sudden onset
- Severe
- Unilateral
- Constant
- Progressively worsening
Nausea + vomiting
Localised tenderness
Potential palpable mass

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143
Q

Diagnosis of ovarian torsion

A

Pelvic ultrasound
Ideally transvaginal USS
‘Whirlpool’ sign = free fluid in pelvis and oedema of the ovary
Definitive diagnosis = laparoscopic surgery

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144
Q

Management of ovarian torsion

A

Emergency –> admit under gynaecology
Laparascopic surgery:
- Detorsion (fixed in place)
- Oophrectomy

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145
Q

Complications of ovarian torsion

A

Loss of function of ovary (typically other compensates)
Necrotic ovary not removed –> infection –> abscess —> sepsis
Rupture –> peritonitis + adhesions

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146
Q

Small for gestational age vs foetal growth restriction

A

SGA = baby small for dates, no reason stated why. Baby may be growing appropriately and not at increased risk of complications
FGR = growth slowed due to pathology, with a higher risk of morbidity and mortality, many end up SGA

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147
Q

Placenta-mediated causes of IUGR

A

Idiopathic
Pre-eclampsia
Maternal smoking
Maternal alcohol
Anaemia
Malnutrition
Infection
Maternal health conditions

Refers to conditions that affect transfer of nutrients across the placenta

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148
Q

Non-placenta mediated causes of IUGR

A

Refers to pathology of foetus

Genetic abnormalities
Structural abnormalities
Foetal infection
Errors of metabolism

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149
Q

Risk factors for IUGR

A

Maternal age <16 or >35
Low BMI
Pre-pregnancy weight >75kg
Low interpregnancy interval (<6 months) or long interval (>120 months)

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150
Q

Risk factors for IUGR

A

Maternal age <16 or >35
Low BMI/Obesity
Diabetes
Low interpregnancy interval (<6 months) or long interval (>120 months)
Pre-existing maternal disease e.g. renal disease, hypertension
Pregnancy complications e.g. pre-eclampsia
Multiple pregnancy
Smoking
Drug use

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151
Q

Signs of IUGR

A

SGA
Reduced amniotic fluid volume
Abnormal Doppler studies (‘head sparing’)
Reduced foetal movements
Abnormal CTGs

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152
Q

Monitoring of SGA/IUGR

A

Women with 3 or more minor/1 or more major risk factors, or with issues measuring symphisis fundal height –> serial growth scans + umbilical artery doppler

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153
Q

Management of IUGR at term

A

Delivered if beyond 36 weeks
Labour induction or C-section are required

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154
Q

Management of IUGR preterm

A

Aim to prevent in utero demise or neurological damage, whilst maximising gestation
Abnormal doppler –> reviewed at least 2x weekly
If absent end-diastolic flow –> admit mother, give steroids if pre-34 weeks, daily CTG
Beyond 34 weeks, delivery often performed

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155
Q

Preterm prelabour rupture of membranes (P-PROM)

A

Amniotic sac has ruptured before onset of labour, and before 37 weeks gestation

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156
Q

Diagnosis of P-PROM

A

Pooling of amniotic fluid in vagina on speculum examination
If doubt of diagnosis –>
- Insulin-like growth factor-binding protein-1: present in high concentrations in amniotic flud, tested on vaginal fluid
- Placental alpha-microglobin-1 (similar alternative)
Ultrasound may be useful - oligohydramnios

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157
Q

Management of P-PROM

A

Prophylactic antibiotics to prevent chorioamnionitis: erythromycin 250mg qds for 10 days, or until labour is established
Induction of labour may be offered from 34 weeks

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158
Q

Options for prophylaxis of preterm labour

A

Vaginal progesterone (gel or pessary) - offered if cervical length <25mm on USS between 16-24GW, with no previous preterm birth/trauma

Cervical cerclage - offered if cervical length <25mm between 16-24GW, with previous premature birth or cervical trauma

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159
Q

When is rescue cervical cerclage offered

A

16-27+6 GW
When there is cervical dilatation without rupture of membranes

160
Q

How is preterm labour with intact membranes diagnosed

A

Regular painful contraction and cervical dilatation without rupture of amniotic sac
<30GW: diagnosis based on clinical assessment
>30GW: TVUS may be used to assess cervical length. >15mm indicates preterm labour unlikely
Test for foetal fibronectin –> <50ng/mL means preterm labour is unlikely

161
Q

Management of preterm labour

A

Foetal monitoring
Tocolysis: nifedipine or atosiban (24-33+6 GW). Used to delay by around 48 hours
Maternal corticosteroids (<35GW)
IV magnesium sulphate (<34GW)
Delayed cord clamping/cord milking at birth

162
Q

Definition of primary amenorrhoea

A

Not starting menstruation:
- By 13 years with no other evidence of pubertal development
- By 15 years where there are other signs of puberty e.g. breast bud development

163
Q

Hypogonadotropic hypogonadism

A

Deficiency of LH and FSH

164
Q

Hypergonadotropic hypogonadism

A

Lack of response to LH and FSH by gonads

165
Q

Causes of hypogonadotropic hypogonadism

A

Hypopituitarism
Damage to hypothalamus or pituitary
Significant chronic conditions e.g. CF or IBD
Excessive exercise or dietng
Constitutional delay in growth + development
Endocrine disorders
Kallman syndrome

166
Q

Causes of hypergonadotropic hypogonadism

A

Previous damage to gonads
Congenital absence of ovaries
Turner’s syndrome

167
Q

Kallman syndrome

A

Genetic condition causing hypogonadotropic hypogonadism with failure to start puberty (deficiency of GnRH)
Associated with anosmia

168
Q

Androgen insensitivity syndrome

A

Condition where tissues are unable to respond to androgen hormones e.g. testosterone
X-linked recessive condition caused by mutation in androgen receptor gene on X chromosome
Excess androgens –> oestrogen –> female secondary sexual characteristics

169
Q

Features of androgen insensitivity syndrome

A

Normal female external genitalia and breast tissue
Testes in abdomen or inguinal canal
Absent uterus, upper vagina, fallopian tubes and oaries
Patients genetically male (XY chromosome)
Taller than female average
Lack of pubic hair, facial hair and male type muscle
Infertile

170
Q

Development of organs in androgen insensitvity syndrome

A

Development of testes is indepedent of androgens
Female internal organs do not develop as testes produce anti-Mullerian hormone –> structures regress
Wolffian ductal structures regress as they require stimulation from androgens

171
Q

Presentation of androgen insensitivity syndrome

A

Inguinal hernias in infancy, containing testes
Or primary amenorrhoea at puberty
Hormone tests:
- Raised LH
- Normal or raised FSH
- normal or raised testosterone (for male)
- Raised oestrogen (for male)

172
Q

Management of androgen insensitivity syndrome

A

Bilateral orchiedectomy - risk of testicular cancer
Oestrogen therapy
Vaginal dilators, or vaginal surgery to create adequate length (if raised as female)
Psychological + social support

173
Q

Management of hypogonadotrophic hypogonadism

A

Pulsatile GnRH can be used to induce ovulation + menstruation: may induce fertility
If pregnancy not wanted, COCP used for replacement sex hormones, to induce menstruation + prevent symptoms of oestrogen deficiency

174
Q

Definition of secondary amenorrhoea

A

No menstruation >3 months after previous regular menstrual periods
Consider assessment and investigation at 3-6 months
If previously infrequent/irregular periods, investigate 6-12 months

175
Q

Causes of secondary amenorrhoea

A

Pregnancy
Menopause + premature ovarian failure
Hormonal contraception
Hypothalamic/pituitary pathology
Ovarian causes e.g. PCOS
Uterine pathology e.g. Asherman’s syndrome
Sheehan’s syndrome
Thyroid pathology
Hyperprolactinaemia

176
Q

Pituitary causes of secondary amenorrhoea

A

Tumours e.g. prolactinoma
Pituitary failure - trauma, radiotherapy, surgery or Sheehan syndrome

177
Q

Hormone tests for secondary amenorrhoea

A

beta-hCG: rule out pregnancy
FSH: high FSH suggests primary ovarian failure
LH: high LH, or LH:FSH ratio suggests PCOS
Prolactin
TSH –> T3/T4
Testosterone: raised –> PCOS, androgen insensitivity syndrome, or congenital adrenal hyperplasia

178
Q

Characteristic features of PCOS

A

Rottersam crtieria means 2/3 present:
Multiple ovarian cysts (or ovarian volume >10cm3)
Oligoovulation/anovulation –> Oligomenorrhoea
Hyperandrogenism (hirsutism or acne)

Insulin resistance

179
Q

Presentation of PCOS

A

Oligomenorrhoea/amenorrhoea
Infertility
Obesity (70%)
Hirsutism
Acne
Hair loss in male pattern

180
Q

Complications of PCOS

A

Insulin resistance + diabetes
Acanthosis nigricans (thickened, rough skin in axilla and on elbows. Velvety texture. Occurs with insulin resistance)
CVD
Hypercholesterolaemia
Endometrial hyperplasia + cancer
OSA
Depression + anxiety
Sexual problems

181
Q

Differential diagnosis of hirsutism

A

Medications: phenytoin, ciclosporin, corticosteroids, testosterone, anabolic steroids
Ovarian or adrenal tumours secreting androgens
Cushing’s syndrome
Congenital adrenal hyperplasia

182
Q

Insulin resistance + androgens

A

Insulin resistance –> increased insulin secretion
Insulin –> release of androgens from ovaries and adrenal glands
Insulin –> supresses sex-hormone binding globulin (normally supresses function of androgens)
–> increased hyperandrogenism
Insulin –> halts development of follicles in ovaries

183
Q

Blood tests in PCOS

A

Testosterone: raised
SHBG
LH: raised, raised LH:FSH ratio
FSH
Prolactin
TSH
Normal, or raised oestrogen
Raised insulin

184
Q

Other investigations for pCOS

A

Transvaginal ultrasound - string of pearls apperance (follicles around periphery of ovaries)
- 12 or more developing follicles in one ovary
- Ovarian volume >10cm3
NB: not reliable in adolescents

75g 2h OGTT for insulin sensitivity
- Impaired fasting glucose = 6.1-6.9mmol/L
- IGT: at 2 hours 7.8-11.1mmol/L
- Diabetes: plasma glucose at 2 hours >11.1mmol/L

185
Q

Management of PCOS

A
  • Reduce risk of complications e.g.
    Weight loss (use orlistat if BMI >30, lipase inhibitor)
    Low GI, calorie-controlled diet
    Exercise
    Smoking cessation
    Antihypertensives when required
    Statins (QRISK>10%)
186
Q

Endometrial cancer + PCOS

A

Usually, corpus luteum releases progesterone after ovulation
Oligo/anovulation in PCOS –> produce oestrogen, not progesterone
If >3 months between periods –> investigate with pelvic ultrasound to assess endometrial thickness (using cyclical progestogens to induce a period prior to USS)

187
Q

How to reduce risk of endometrial cancer e.g. in PCOS

A

Mirena coil
Inducing a withdrawal bleed at least every 3-4 months:
- Cyclical progestogens e.g. medrocyprogesterone acetate 10mg od for 14 days
- COCP

188
Q

Action of metformin in PCOS

A

Appetite reduction
Decreased LH from anterior pituitary –> decreased androgen production from theca cells + decreased oestrogen production –> follicular development
Increased sex-hormone binding globulin in the liver –> decreased free androgens

189
Q

Options for infertility management in PCOS

A

Weight loss –> restore regular ovulation
Clomifene
Laparascopic ovarian drilling
IVF

Metformin + letrozole may also help restore ovulation

Screening for GDM if pregnant

190
Q

Hirsutism management

A

Weight loss
Co-cyprindiol is a COCP used for hirsutism and acne - increased risk of VTE –> stopped after 3 months
Topical eflornithine for facial hirsutism. Takes 6-8 weeks, hirsutism will return within 2 months of stopping

Electrolysis/laser hair removal
Spironolactone
Finasterine
Flutamide
Cyproterone acetate

191
Q

Normal function of Bartholin’s glands

A

Produce mucus to help with vaginal lubrication

192
Q

Presentation of Bartholin cyst

A

Swelling (ususally unilateral)
Tender
Fluid-filled cyst 1-4 cm

193
Q

Complication of Bartholin cyst

A

Bartholin’s abscess
Hot, tender, red + potentially draning pus

194
Q

Management of Bartholin’s cyst

A

Good hygeine
Analgesia
Warm compresses
Incision avoided due to recurrence
Biopsy if vulval malignancy needs to be excluded

195
Q

Management of Bartholin’s abscess

A

Antibiotics
Swab of pus - culture + sensitivities
Swab for chlamydia + gonorrhoea
Surgical management if required
- Word catheter (local)
- Marsupialisation (general)

196
Q

Age mostly affected by cervical cancer

A

Women <35
Typically women of reproductive age

197
Q

Virus associated with cervical cancer

A

Human papillomavirus (HPV)
Types 16 + 18 particularly associated + targeted with HPV vaccine

198
Q

Risk factors for cervical cancer

A

Early sexual activity
Increased number of sexual partners (esp if they have had more partners)
Not using condoms
Non-engagement with screening
Smoking
HIV
COCP >5 years
Increased number of full-term pregnancies
FHx
Exposure to diethylstilbestrol during foetal development

199
Q

Presentation of cervical cancer

A

During smear if asymptomatic
Abnormal vaginal bleeding: intermenstrual, postcoital, post-menopausal
Vaginal discharge (purulent, red-brown)
Pelvic pain
Dyspareunia

200
Q

Concerning appearances of cervix

A

Ulceration
Inflammation
Bleeding
Visible tumour

201
Q

Diagnosis of cervical intraepthelial neoplasia/cervical cancer

A

Colposcopy, not on smear test
+/- biopsy

202
Q

Grades of cervical intraepithelial neoplasia

A

CNI: mild, affects 1/3 thickness, likely to return to normal without treatment
CNII: moderate dysplasia, affects 2/3 thickness, likely to progress to cancer if untreated
CNIII: severe dysplasia, very likely to progress (sometimes called cervical carcinoma in situ)

203
Q

What does a smear test look at

A

Precancerous changes (dyskaryosis)
Cells from cervix transported using liquid-based cytology
Samples initially tested for high-risk HPV

204
Q

Who is invited to cervical screening

A

Women aged 25-49: every three years
Women aged 50-64: every five years
Women with HIV: screened annually
Women >65: if they have not been screened since 50, or with recent abnormal smears

205
Q

Outcome if HPV positive but cytology normal on cervical screening

A

Repeat HPV test after 12 months

206
Q

Most common types of cervical cancer

A

Squamous cell carcinoma (70-80%)
Adenocarcinoma (10%)

207
Q

What is cervical intraepithelial neoplasia

A

Cervical dysplasia/dyskaryosis
Abnormal growth of cervical mucosa
Porentially pre-malignant
Mostly result of HPV infection

208
Q

Management of dyskaryosis if HPV negative

A

Return to normal screening recall

209
Q

Management of dyskaryosis if HPV positive

A

Refer for colposcopy due to increased risk of histological abnormality

210
Q

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
Lymph nodes can be involved at any stage

211
Q

Management of Stage 1a cervical cancer/CIN

A

Large loop excision of the transformation zone (LLETZ) or cone biopsy

212
Q

Management of Stage 1b-2a cervical cancer

A

Radical hysterectomy
Removal of local lymph nodes (chemo and radiotherapy)

213
Q

Management of stage 2b-4a cervical cancer

A

Chemotherapy + radiotherapy

214
Q

Management of stage 4b cervical cancer

A

Combination of surgery, radiotherapy, chemotherapy + palliative care

215
Q

Important facts about HPV vaccine

A

Strains 6 + 11 (genital warts), and 16 +18 (cervical cancer) covered
Given before sexually active (girls + boys aged 12-13)
2 doses required

216
Q

Main form of endometrial cancer

A

Adenocarcinoma (80%)
Oestrogen-dependent

217
Q

Risk factors for endometrial cancer

A

Consider as exposure to unopposed oestrogen
Increased age
Earlier onset menstruation
Late menopause
Oestrogen-only HRT
No or fewer pregnancies
Obesity (oestrogen in aipose tissue, and aromatase to convert androgens into oestrogen))
PCOS
Tamoxifen
Diabetes (type 2)
HNPCC or Lynch syndrome

218
Q

Protective factors against endometrial cancer

A

COCP
Mirena coil
Increased pregnancies
Cigarette smoking (in postmenopausal women)

219
Q

Presentation of endometrial cancer

A

POSTMENOPAUSAL BLEEDING (endometrial cancer until proven otherwise)
Postcoital or intermenstrual bleeding
Unusually heavy menstrual bleeding
Abnormal vaginal discharge
Haematuria
Anaemia
Raised platelet count

Pain + discharge are unusual

220
Q

Investigations for endometrial cancer

A

TVUSS - endometrial thickness (<4mm post-menopause)
Pipelle biopsy - highly sensitive
Hysteroscopy (with endometrial biopsy)

221
Q

Management for endometrial cancer

A

Total abdominal hysterectomy with bilateral salpingo-oophrectomy
Involves removing pelvic lymph nodes, surrounding tissues + top of vagina

Potential of: radiotherapy, chemotherapy, progesterone (slow progression of the cancer) in women not suitable for surgery

222
Q

What is lichen sclerosus

A

Chronic, inflammatory, progressive skin disorder that most commonly affects the genitalia and perianal area

223
Q

Epidemiology of lichen sclerosus

A

Women > Men
Two peaks of onset: prepubertal, peri- or post-menopausal woman
Can be associated with autoimmune diseases: type 1 diabetes, alopecia, hypothyroid an vitiligo

224
Q

Presentation of lichen sclerosus

A

Typical = women aged 45-60 years
Vulval itching
Skin changes in vulva
Can be asymptomatic
Soreness + pain possibly worse at night
Skin tightness
Superficial dyspareunia
Erosions
Fissures

225
Q

What is the Koebner phenomenon

A

Refers to when signs and symptoms are made worse by friction to the skin e.g. with lichen sclerosus

226
Q

Appearance of skin in genital area in lichen sclerosus

A

Affects labia, perianal and perineal skin
Fissures, cracks, erosions or haemorrhages under the skin
‘Porcelain-white’ in colour
Shiny
Tight
Thin
Slightly raised
Papules or plaques

227
Q

Management of lichen sclerosus

A

Potent topical steroids e.g. clobetasol propionate (dermovate) - gradually reduced in frequency
Emollients

228
Q

Complications of lichen sclerosus

A

Squamous cell carcinoma of the vulva
Pain + discomfort
Sexual dysfunction
Bleeding
Narrowing of vaginal or urethral openings

229
Q

What is a hydatidiform mole

A

Tumour that grows like pregnancy inside uterus - molar pregnancy

230
Q

How is a complete mole formed

A

Two sperm cells fertilise an ovum with no genetic material
Sperm combine genetic material –> cells divide –> complete mole, with no foetal material

231
Q

How is a partial mole formed

A

Two sperm cells fertilise a normal ovum –> three sets of chromosomes
Cell divides –> tumour (partial mole), some foetal material may form

232
Q

Presentation of molar pregnancy vs normal pregnancy

A

More severe morning sickness
Vaginal bleeding
Increased enlargement of uterus
Abnormally high hCG
Thyrotoxicosis

233
Q

Diagnosis of molar pregnancy

A

Pelvic ultrasound –> snowstorm apperance of pregnancy
Confirmed on histology after evacuation

234
Q

Management of molar pregnancy

A

Evacuation of uterus
Histological examination of products of conception
Referral to gestational trophoblastic disease centre
Monitor hCG levels
Chemo if mole has metastasised

235
Q

What is adenomyosis

A

Endometrial tissue within the myometrium
More common in later reproductive years + in multiparous women

236
Q

Presentation of adenomyosis

A

Dysmennorhoea
Menorrhagia
Dyspareunia
Infertility or pregnancy-related complications

Tender + enlarged uterus (softer than with fibroids)

237
Q

Investigation of adenomyosis

A

1st line: TVUS
MRI + transabdominal USS suitable alternatives
Gold standard: histological examination of uterus after hyseterectomy

238
Q

Management

A

Symptoms tend to resolve after menopause
Not wanting contraception:
- Tranexamic acid (no associated pain)
- Mefenamic acid (associated pain)
Contraception acceptable:
- Mirena coil
- COCP
- Cyclical oral progestogens
Others:
- GnRH analogues
- Endometrial ablation
- Uterine artery embolisation
- Hysterectomy

239
Q

Problems associated with adenomyosis in pregnancy

A

Infertility
Miscarriage
Preterm birth
SGA
P-PROM
Malpresentation
C-section
PPH

240
Q

Uterine prolapse

A

Uterus descends into vagina

241
Q

Vault prolapse

A

Occurs in women who have had a hysterectomy
Top of vagina descends into vagina

242
Q

Rectocele

A

Defect in posterior vaginal wall -> rectum prolapses forward into vagina

243
Q

Complications of rectocele

A

Foecal loading –> constipation, urinary retention, palpable lump in vagina (women may press lump backwards to allow opening of bowels)

244
Q

Cystocele

A

Defect in anterior vaginal wall
Bladder prolapses backwards into vagina
–> urinary symptoms

245
Q

Urethrocele

A

Prolapse of urethra

246
Q

Cystourethrocele

A

Prolapse of bladder + urethra

247
Q

Risk factors for pelvic organ prolapse

A

Multiple vaginal deliveries (especially if instrumental, prolonged, or traumatic)
Advanced age/postmenopausal
Obesity
COPD (coughing)
Chronic constipation (straining)

248
Q

Presentation of pelvic organ prolapse

A

Feeling of something coming down in vagina
Heavy sensation in pelvis
Urinary symptoms
Bowel symptoms
Sexual dysfunction
Lump or mass felt by women in vagina - may be pushing it back themselves

249
Q

Examination of pelvic organ prolapse

A

Ideally empty bladder and bowels
Dorsal and left lateral positions may be used
Sim’s speculum - used to support vaginal wall while other walls are examined
Woman may cough or ‘bear down’ to assess full descent

250
Q

Severity of uterine prolapse

A

Pelvic organ prolapse quantification (POP-Q)
0 = normal
1 = lowest part >1cm above introitus
2 = lowest part within 1cm of introitus
3 = lowest part >1cm below introitus
4 = full descent with eversion of vagina

251
Q

Conservative management of pelvic organ prolapse

A

Women coping with mild symptoms, don’t tolerate pessaries, or not a candidate for surgery
Physiotherapy for pelvic floor
Weight loss
Lifestyle changes for stress incontinence e.g. reduced caffeine intake/incontinence pads
Treatment of related symptoms eg. anticholinergic medications for stress incontinence
Vaginal oestrogen cream

252
Q

Pessaries for pelvic organ prolapse

A

Ring - sit around cervix, holding uterus up
Shelf/Gellhorn - flat disc with stem, sit below uterus with stem pointing downwards
Cube
Donut
Hodge - rectangular almost. One side hooked around posterior aspect of cervix, other extends into vagina
Should be removed + cleaned/changed periodically (e.g. every 4 months)
Can cause vaginal irritation + erosion –> oestrogen cream

253
Q

Surgery for pelvic organ prolapse

A

Definitive option
Many options incl. hyesterectomy
Complications
- Pain, bleeding, infection, DVT, risk of anaesthetic
- Damage to bladder or bowel
- Recurrence
- Altered experience of sex

254
Q

Mesh repairs for pelvic organ prolapse

A

Now avoided completely
Complications:
- Chronic pain
- Altered sensation
- Dyspareunia (women or her partner)
- Abnormal bleeding
- Urinary or bowel problems

255
Q

Commonest type of vulval cancer

A

Squamous cell carcinoma
(can be malignant melanomas, these are usually pigmented)

256
Q

Risk factors for vulval cancer

A

Advanced age (>75)
Immunosuppression
HPV infection
Lichen sclerosus

257
Q

What is vulval intraepithelial neoplasia

A

Premalignant condition of squamous epithelium - often white or plaque-like
High grade squamous intraepithelial lesion: associated with HPV infection, typically occurs in women aged 35-50 years
Differentiated VIN: associated with lichen sclerosus, aged 50-60 years
Diagnosed on biopsy
Managed by watch + wait, wide local excision, imiquimod cream, or laser ablation

258
Q

Presentation of vulval cancer

A

Vulval lump
Ulceration
Bleeding
Pain
Itching
Groin lymphadenopathy

Appearance of labia majora (typically affected):
- Irregular mass
- Fungating lesion
- Ulceration
- Bleeding

259
Q

Management of vulval cancer

A

2WW
Biopsy of lesion, sentinel node biopsy, and imaging for staging
Depend on stage:
- Wide local excision to remove cancer
- Groin lymph node dissection
- Chemo
- Radio

260
Q

What is Asherman’s syndrome

A

Adhesions form within uterus, following damage to the uterus
These form physical obstructions + distort pelvic organs –> menstruation abnormalities, infertility + recurrent miscarriages

261
Q

What may lead to Asherman’s syndrome

A

Pregnancy-related dilatation and curettage procedure e.g. treatment of retained POC
Uterine surgery e.g. myomectomy
Pelvic infection

262
Q

Presentation of Asherman’s syndrome

A

Presents following recent dilatation + curettage, uterine surgery or endometritis
Secondary amenorrhoea
Significantly lighter periods
Dysmenorrhoea
Infertility

263
Q

Diagnosis of Asherman’s syndrome/intrauterine adhesions

A

Gold standard: hysteroscopy (can dissect + treat adhesions)
Hysterosalpingography
Sonohysterography (uterus filled with fluid for pelvic USS)
MRI scan

264
Q

Management of Asherman’s syndrome

A

Dissect adhesions during hysteroscopy
Recurrence after treatment is common

265
Q

What is shoulder dystocia

A

A complication of vaginal cephalic delivery
Inability of the body of the foetus to be delivered using gentle traction once head has been delivered
Usually due to impaction of anterior foetal shoulder on maternal pubic symphysis
Head may remain face downwards and not turn sidewayds

266
Q

Risk factors for shoulder dystocia

A

Foetal macrosomia
High maternal BMI
Diabetes mellitus
Prolonged labour

267
Q

Management of shoulder dystocia

A

Call for senior help
McRoberts’ manoeuvre
Episiotomy may be required to allow better access for internal manoeuvres
Pressure to anterior shoulder by pressing on suprapubic area

268
Q

What is McRoberts manoeuvre

A

Flexion + abduction of maternal hips (bringing thighs towards abdomen)
Increases anterior-posterior angle of pelvis (posterior pelvic tilt)

269
Q

Rubins manoeuvre for shoulder dystocia

A

Reach into vagina to put pressure on psoterior aspect of baby’s anterior shoulder - aid it to move under pubic symphysis

270
Q

Wood’s screw manoeuvre for shoulder dystocia

A

Performed during Rubins
Other hand reaches into vagina to put pressure on anterior aspect of posterior shoulder - rotates baby
(top shoulder forwards, bottom shoulder back)
Reverse can be tried if this does not wor

271
Q

Zavanelli manoeuvre

A

Pushing baby’s head back into vagina to allow delivery by emergency c-section

272
Q

Complications of shoulder dystocia

A

Foetal hypoxia –> cerebral palsy
Brachial plexus injury + Erb’s palsy
Perineal tears
PPH

273
Q

Normal thickness of endometrium

A

<5mm

274
Q

What is endometrial hyperplasia

A

Abnormal proliferation of endometrium (>normal proliferation during menstrual cycle)
Can be considered a pre-malignant condition

275
Q

Management of endometrial hyperplasia

A

Simple, without atypia: high dose progestogens, repeat sampling in 3-4 months. Mirena may be used
Atypia: hysterectomy usually advised

276
Q

What ovarian tumour is associated with development of endometrial hyperplasia

A

Granulosa cell tumours

277
Q

Factors associated with endometrial hyperplasia

A

Taking oestrogen unopposed by progesterone
Obesity
Late menopause
Early menarche
Aged >35
Current smoker
Nulliparity
Tamoxifen (anti-oestrogen on breast, pro-oestrogen on uterus + bones)

278
Q

Investigation of post-menopausal bleeding

A

1st: TVUSS +/- endemotrial pipelle biopsy
If inconclusive results –> hysteroscopy + biopsy (dilation + curettage)

279
Q

Which ovarian tumours are associated with an increased production of hormones

A

Thecoma
Fibroma
Sertoli cell
Granulosa cell

280
Q

Who is eligible for a vaginal birth after caesarean

A

Planned VBAC appropriate if:
- >/= 37 weeks gestation
- Single previous Caesarean delivery
Absolute contraindications: previous uterine rupture, classical (vertical) scar

281
Q

Category 1 C-section

A

Immediate threat to life of mother or baby
Delivery of baby should occur within 30 minutes of decision
e.g. suspected uterine rupture, major placental abruption, cord prolapse, foetal hypoxia, persistent foetal bradycardia

282
Q

Category 2 C-section

A

Maternal or foetal compromise, not immediately life-threatening
Delivery within 75 minutes of decision

283
Q

Category 3 C-section

A

Delivery required, mother and baby are stable

284
Q

Category 4 C-section

A

Elective

285
Q

Indications for Caesarean-section

A

Absolute cephalopelvic disproportion
Placenta praevia (grades 3/4)
Pre-eclampsia
Post-maturity
IUGR
Foetal distress in labour/prolapsed cord
Failure to progress
Brow malpresentation
Placental abruption (if foetal distress. Dead –> deliver vaginally)
Vaginal infection e.g. active herpes
Cervical cancer
HIV with high viral load/not receiving any anti-retroviral therapy
Hep C (only if co-infected with HIV)
Twin pregnancy where first baby is breech

286
Q

Investigations in menorrhagia

A

FBC
TVUS if symptoms suggest structural or histological abnormality e.g. intermenstrual/postcoital bleeding, pelvic pain, pressure symptoms

287
Q

Management of menorrhagia, not requiring contraception

A

Mefenamic acid 500mg tds (if painful)
Tranexamic acid 1g tds
Both started on first day of period

288
Q

Management of menorrhagia (+contraception)

A

1st line: intrauterine system (mirena)
COCP
Long-acting progestogens

289
Q

Short-term option for HMB

A

Norethisterone 5mg tds

290
Q

Normal foetal heart rate on CTG

A

110-160bpm
Tachycardia –> prematurity, hypoxia, foetal distress, maternal pyrexia or beta-agonists
Bradycardia –> severe foetal distress, foetal hypoxia or acidaemia
<90 sustained –> impending foetal demise

291
Q

Normal foetal HR variability on CTG

A

Reassuring: 5-25bpm
Non-reassuring:
- <5bpm for 30-50 minutes
- >25bpm for 15-25 minutes
Abnormal:
- <5bpm for >50 minutes
- >25bpm for >25 minutes
- Sinusoidal

292
Q

Interpreting accelerations on CTG

A

Accelerations = abrupt increase in baseline HR of >15bpm for >15 seconds
Presece of accelerations is reassuring - especially if they occur alongside uterine contractions
Absence is not concerning if the rest of the CTG is normal

293
Q

Decelerations on CTG

A

Abrupt decrease in baseline HR of >15bpm fr >15 seconds

294
Q

Early decelerations on CTG

A

Start when contractions begin, recover when they stop
Due to increased foetal intracranial pressure causing increased vagal tone
Physiological, not pathological

295
Q

Variable decelerations on CTG

A

Rapid fall in baseline heart rate with variable recovery phase
May not have any relationship to uterine contractions
Most commonly caused by umbilical cord compression - may show acceleration followed by deceleration followed by acceleration (decels without these ‘shoulders’ are more concerning)
Foetus is not yet hypoxic, but needs close monitoring

296
Q

Late decelerations on CTG

A

Decels begin at peak of contraction, and recover after contraction ends
Indicates insufficient blood flow to uterus and placenta –> foetal hypoxia + acidosis
e.g. maternal hypotension, pre-eclampsia or uterine hyperstimulation

297
Q

Prolonged deceleration on CTG

A

> 2 minutes
2-3 minutes = non-reassuring
3 minutes = abnormal

298
Q

Sinusoidal pattern on CTG

A

Smooth, regular, wave-like pattern
2-5 cycles a minute
Stable baseline around 120-160bpm
No beat to beat variability
Usually indicates:
- Severe foetal hypoxia
- Severe foetal anaemia
- Foetal/maternal haemorrhage

299
Q

Non-reassuring features of decelerations on CTG

A

Variable with no concerning characteristics for 90+ minutes
Variable with any concerning characteristics in up to 50% of contractions for 30+ mins
Variable with any concerning characteristics in >50% contractions for <30 mins
Late decels in >50% contractions for <30 mins with no maternal/foetal clinical risk factors e.g. vaginal bleeding or significant meconium

300
Q

Abnormal features of decelerations on CTG

A

Variable with any concerning characteristics in >50% of contractions for 30 minutes (less if any risk factors)
Late decels for 30 minutes (less with risk factors)
Acute bradycardia, or a single prolonged decel lasting 3 minutes or more

301
Q

Concerning characteristics of variable decelerations on CTG

A

> 60 seconds
Reduced baseline variability within the deceleration
Failure to return to baseline
Biphasic (W) shape
No shouldering

302
Q

Folic acid supplementation in pregnancy

A

All women - 400mcg of folic acid until 12th week
Women at higher risk of conceiving a child with nueral tube defects: 5mg of folic acid before conception, until 12th week of pregnancy

303
Q

Who is considered higher risk for neural tube defect during pregnancy

A

Either partner has had a NTD
Previous pregnancy affected by NTD
Family history of NTD
Antiepileptic drugs
Coeliac disease, diabetes, or thalassaemia trait
Woman is obese (>30 BMI)

304
Q

Definition of premature ovarian insufficiency

A

Onset of menopausal symptoms + elevated gonadotrophin levels <40 years old

305
Q

Causes of premature menopause

A

Idiopathic
Bilateral oophrectomy
Radiotherapy
Chemotherapy
Infection e.g. mumps
Autoimmune disorders
Resistant ovary syndrome (FSH receptor abnormalities)

306
Q

Presentation of premature menopause

A

Similar to normal climacteric features
- Hot flushes
- Night sweats
Infertility
Secondary amenorrhoea
Raised FSH, LH levels
Low oestradiol

307
Q

Blood tests for hormones in menopause/premature menopause

A

FSH >40 iu/L
- Elevated levels should be demonstrated on 2 blood samples, taken 4-6 weeks apart
Low oestradiol <100 pmol/L
High FSH seen due to decreased oestrogen –> decreased negative feedback on pituitary

308
Q

Management of premature menopause

A

HRT/COCP until age of average menopause (51 years)
Sequential/cyclical HRT recommended for endometrial protection if they have a uterus

309
Q

Definition of puerperal pyrexia

A

Temperature >38 degrees
In first 14 days following delivery

310
Q

Causes of puerperal pyrexia

A

Endometritis - most common
UTI
Wound infections
Mastitis
Venous thromboembolism

311
Q

Management of puerperal pyrexia

A

If endometritis suspected –> refer to hospital for IV antibiotics
- clindamycin + gentamicin until afebrile >24 hours

312
Q

Dermoid cyst

A

Benign germ cell tumours
May contain skin appendages, hair + teeth
Most common bening ovarian tumour in women <30 years
Usually asymptomatic
Torsion is more likely than with other tumours

313
Q

Use of levonorgestrel as emergency contraception

A

Should be taken ASAP
Must be taken within 72 hours of unproected sexual intercourse
Single dose 1.5mg (doubled if BMI >26, or weight >70kg)
Repeated dosing possible
Can restart hormonal contraception immediately

314
Q

Use of ulipristal as emergency contraception

A

Selective progesterone receptor modulator
EllaOne
30mg oral dose ASAP - no later than 120 hours after intercourse
May reduce effectiveness of hormonal contraception - wait 5 days before restarting
Breastfeeding should be delayed for 1 week
Repeated dosing possible

315
Q

Use of copper IUD as emergency contraception

A

Most effective method: should be offered to all women who meet criteria
Must be inserted within:
- 5 days of unprotected sexual intercourse
- OR 5 days after the likely ovulation date (if >5 days since UPSI)
May inhibit fertilisation or implantation
Prophylactic antibiotics given if high risk for STIs
May be left in situ for futue protection

316
Q

Umbilical cord prolapse

A

Umbilical cord descends ahead of presenting part of the foetus

317
Q

Complications of untreated umbilical cord prolapse

A

Compression of the cord, or cord spasm
–> fetal hypoxia
–> irreversible damage or death

318
Q

Risk factors for umbilical cord prolapse

A

Prematurity
Multiparity
Polyhydramnios
Twin pregnancy
Cephalopelvis disproportion
Abnormal presentations

319
Q

Management of cord prolapse

A

Presenting part of foetus may be pushed back into uterus to avoid compression
If past level of introitus: minimal handling, kept warm and moist to avoid vasospasm
Patient on all fours (or left lateral) whilst emergency c-section is prepaed
Tocolytics may be used
Retrofilling of bladder - may be helpful as gently elevates presenting part
Delivery: usually C-section, intrumental possible if head low and cervix fully dilated

320
Q

Associations with hyperemesis gravidarum

A

Multiple pregnancies
Trophoblastic disease e.g. molar pregnancy
Hyperthyroidism
Nulliparity
Obesity

Smoking associated with decreased incidence

321
Q

Triad for diagnosis of hyperemesis gravidarum

A

5% pre-pregnancy weight loss
Dehydration
Electrolyte imbalance

322
Q

Management of hyperemesis

A

Antihistamines = 1st line
- Oral cyclizine/promethazine
- Oral prochlorperazine = alternative
Ondansetron + metoclopramide = 2nd line
- Ondansetron –> risk of cleft-lip/palate
- Metoclopramide –> EPSEs, not used >5 days
Ginger
P6 (wrist) acupressure
Admission may be needed for IV hydration

323
Q

Complications of hyperemesis

A

Wernicke’s encephalopathy
Mallory-Weiss tear
Central pontine myelinolysis
Acute tubular necrosis
SGA foetus
Pre-term birth

324
Q

Testosterone therapy and pregnancy

A

Testosterone therapy in transgender males does not protect against pregnancy
If patient becomes pregnant, testosterone is contraindicated as it can have teratogenic effects

325
Q

Mechanism of action of IUS

A

Levonorgestrel prevents endoemtrial proliferation + causes cervical mucous thickening

326
Q

Potential problems associated with IUS insertion

A

First 6 months: irregular, frequent uterine bleeding, and spotting
Uterine perforation
Ectopic pregnancy
Infection
Expulsion

327
Q

Definition of postpartum haemorrhage

A

Blood loss of 500ml after vaginal delivery
Primary PPH: occurs within 24 hours

328
Q

Causes of primary PPH

A

Tone: uterine atony is the most common cause
Trauma e.g. perineal tear
Tissue e.g. retained placenta
Thrombin e.g. clotting/bleeding disorder

329
Q

Initial management of primary PPH

A

Senior help
ABC approach
- Two, large bore peripheral cannulae
- Lie woman flat
- Bloods including group + save
- Commence warmed crystalloid infusion
Mechanical - rub fundus to stimulate contractions, catheterisation

330
Q

Medical management of primary PPH

A

Medical:
- IV oxytocin (slow IV injection, followed by IV infusion)
- Ergoemtrine (slow IV or IM, unless history of hypertension
- Carboprost IM (unless history of asthma)
- Misoprostol sublingual

331
Q

Surgical management of primary PPH

A

Intrauterine balloon tamponade - if uterine atony only/main cause of haemorrhage
B-Lynch suture
Ligation of uterine arteries or internal iliac arteries
Hysterectomy may be performed as a life-saving procedure

332
Q

Management of chickenpox exposure in pregnancy

A

Check maternal blood for varicella antibodies
If not immune –>
If = 20 weeks gestatation, give varicella-zoster immunoglobulin (single dose) ASAP (within 10 days)
If >20 GW, give either VZIG or oral antivirals 7-14 days after exposure
If >20 GW, presenting within 24 hours of rash, oral aciclovir may be useful

333
Q

Risks of chickenpox exposure in pregnancy

A

Mother: greater risk of pneumonitis
Foetus: foetal varicella syndrome, shingles in infancy, severe neonatal varicella

334
Q

Features of foetal varicella syndrome

A

Dermatomal skin scarring
Neurological deficits
Foetal growth retardation
Limb hypoplasia
Eye defects
Hydrops fetalis

335
Q

What is pre-eclampsia

A

Seen after 20 weeks gestation
Pregnancy-induced hypertension
With proteinuria (sign of end-organ dysfunction)
Oedema

336
Q

What is eclampsia?

A

Development of seizures in association with pre-eclampsia

337
Q

Definition of pregnancy induced/gestational hypertension

A

New onset HTN presenting after 20 weeks’ gestation, without significant proteinuria

338
Q

Risk factors for pre-eclampsia

A

High risk: Pre-existing hypertension
Previous hypertension in pregnancy
Existing autoimmune conditions
Diabetes
CKD
Moderate risk: >40 years old
Obesity
>10 years since previous pregnancy
Multiple pregnancy
First pregnancy
FHx pre-eclampsia

339
Q

Prophylaxis for pre-eclampsia

A

Aspirin: from 12 GW until birth
If one high-risk, or more than one moderate-risk factors

340
Q

Symptoms of pre-eclampsia

A

Headache
Visual disturbance/blurriness (papilloedema)
Nausea + vomiting
Upper abdominal/epigastric pain
Oedema (especially facial)
Reduced urine output
Hyperreflexia

341
Q

Diagnosis of pre-eclampsia

A

Systolic >140mmHg, Diastolic >90mmHg
PLUS one of:
- Proteinuria
- Organ dysfunction e.g. raised creatinine, elevated liver enzymes, seizures, thrombocytopenia, or haemolytic anaemia
- Placental dysfunction e.g. foetal growth restriction, or abnormal Doppler studies

342
Q

Quantifying proteinuria

A

Urine protein:creatinine ratio (>30mg/mmol)
Urine albumin:creatinine ratio (>8mg/mmol)

343
Q

Management of gestational hypertension (no proteinuria)

A

Treat: aim for BP <135/85
Admission if BP >160/110
Weekly urine dipsticks, blood tests
Serial growth scans
Placental growth factor (PlGF) testing

344
Q

Principles of management of pre-eclampsia

A

Scoring to decide whether to admit: fullPIERS, PREP-S
BP monitoring (at least every 48 hours)
USS monitoring performed two weekly

345
Q

Medical management of pre-eclampsia

A

Urgent referral to obstetrics
1st line anti-hypertensive: labetolol (cannot give in asthma, HF or heart block)
2nd line: modified-release nifedipine
3rd line: methyldopa (needs to be stopped within 2 days of birth)
IV hydralazine - in critical care
IV magnesium sulphate - given during labour, and in 24 hours after to prevent seizures
Fluid restriction if severe, to avoid fluid overload

346
Q

Management of gestational hypertension/pre-eclampsia after delivery

A

Enalapril
Nifedipine or amlodipine (1st line in black African or Caribbean patients)
Labetolol/atenolol (3rd line)

347
Q

HELLP syndrome

A

Haemolysis
Elevated Liver enzymes
Low Platelets

348
Q

Timing of booking visit

A

8-12 weeks (ideally <10 weeks)

349
Q

Purpose of booking visit

A

General information e.g. diet, alcohol, smoking etc
BP, Urine dipstick, BMI
Booking bloods/urine:
- FBC, blood group, rhesus status, red cell alloantibodies, haemoglobinopathies
- Hep B, syphilis
- HIV testing offered
- Urine culture for asymptomatic bacteriuria

350
Q

Dating scan

A

10-13+6 weeks
Accurate gestational age calculated from crown rump length
Exclude multiple pregnancy

351
Q

Timing of Down’s syndrome screening

A

11-13+6 weeks
Including nuchal scan

352
Q

Anomaly scan

A

18-20+6 weeks

353
Q

Checkpoints for fundal level

A

Umbilicus - 20 weeks
Xiphoid sternum - 36 weeks

354
Q

Factors associated with an increased risk of miscarriage

A

Increased maternal age
Smoking in pregnancy
Alcohol consumption
Recreational drug use
High caffeine intake
Obesity
Infections + food poisoning
Health conditions
Medications
Unusual shape/structure of womb
Cervical incompetence

355
Q

When are foetal movements normally felt first

A

18-20 weeks (or 16-18 weeks in multiparous women)
If no movement by 24 weeks, referral should be made to maternal foetal medicine unit

356
Q

Risk factors for reduced foetal movements

A

Posture e.g. felt more when lying down, less when standing
Distraction
Placental position e.g. anterior placenta
Medication e.g. alcohol + sedative medications
Foetal position e.g. anterior foetal position
Body habitus - obese patients less likely to feel prominent movements
Amniotic fluid volume - oligo/polyhydramnios can cause reduction
Foetal size - RFM more common in women with SGA foetus

357
Q

Combined test for Down’s syndrome screening

A

Done between 11-13+6 weeks
Nuchal translucencey: thickened
Serum beta-hCG: increased
Pregnancy associated plasma protein A: decreased

358
Q

Quadruple test for Down’s syndrome screening

A

Offered if women book later in pregnancy: done between 15-20 weeks
Alpha-fetoprotein: decreased
Unconjugated oestriol: decreased
hCG: increased
Inhibin A: increased

359
Q

Findings on quadruple test suggestive of Edward’s syndrome

A

Alpha feto-protein: decreased
Unconjugated oestriol: decreased
hCG: decreased
Inhibin A: normal

360
Q

Testing for genetic anomaly diagnosis e.g. of Down’s syndrome

A

Chorionic villous sampling
- 11-14 GW (not performed before 9-11 weeks)
- 1% risk of miscarriage
- Abnormal results due to placental mosaicism –> amniocentesis
Amniocentesis
- Performed >14 GW due to higher chance of talipes
Non-invasive prenatal testing
- Not technically diagnostic so CVS or amniocentesis may sstill be performed

361
Q

Methotrexate and pregnancy

A

Methotrexate should be stopped at least 6 months before conception
Both partners should stop taking methotrexate - not just the woman

362
Q

Use of COCP postpartum

A

Absolutely contraindicated if <6 weeks postpartum, and breastfeeding
- Reduces breast milk volume
UKMEC 2 if breastfeeding 6 weeks-6 months postpartum
Should not be used in first 21 days due to increased VTE risk post-partum
After day 21, additional contraception should be used for first 7 days

363
Q

Use of POP postpartum

A

Can be started any time postpartum, regardless of breastfeeding status
After day 21, additional contraception should be used for first 2 days

364
Q

Use of IUD/IUS postpartum

A

Can be inserted within 48 hours of childbirth, or after 4 weeks

365
Q

After giving birth, when do women require contraception

A

After day 21

366
Q

Presentation of overflow urinary incontinence

A

Incontinence
Voiding symptoms: straining, poor flow, incomplete emptying of bladder
Palpable bladder after voiding
On urodynamics: increased voiding detrusor pressure, decreased pek flow rate

367
Q

Risk factors for amniotic fluid embolism

A

Increasing maternal age
Induction of labour
Caesarean section
Multiple pregnancy

368
Q

Presentation of amniotic fluid embolism

A

Usually presents at labour + delivery, but can be postpartum
Acute onset
SOB
Hypoxia
Hypotension
Coagulopathy
Haemorrhage
Tachycardia
Confusion
Seizures
Cardiac arrest

369
Q

Management of amniotic fluid embolism

A

Supportive - ABCD
A - secure airway
B - oxygen for hypoxia
C - IV fluids for hypotension, blood transfusion in haemorrhage
D - treat seizures + consider other deficits

370
Q

Risk factors for transverse lie

A

Multiparity
Fibroids/other pelvic tumours
Multiple pregnancy
Prematurity
Polyhydramnios
Foetal abnormalities
Placenta praevia

371
Q

Management of transverse lie

A

<36 weeks: no management required
>36 weeks:
- Active management = external cephalic version, performed as long as membranes have not been ruptured. Contraindicated in multiple pregnancy, or major uterine abnormality
- Elective caesarean

372
Q

Complete (flexed) breech

A

Both legs flexed at hips and knees
Foetus appears ‘cross-legged’

373
Q

Frank (extended breech)

A

Both legs flexed at hip and extended at knee
Most common type of breech presentation

374
Q

Footling breech

A

One or both legs extended at the hip so that the foot is the presenting part

375
Q

Risk factors for breech presentation

A

Majority are chance occurences
Uterine risk factors:
- Multiparity
- Uterine malformations e.g. septate uterus
- Fibroids
- Placenta praevia
Foetal risk factors:
- Prematurity
- Macrosomia
- Polyhydramnios
- Multiple pregnancy
- Abnormality e.g. anencephaly

376
Q

Management of breech presentation

A

ECV (external cephalic version): offered from 37 weeks, or 36 in primiparous women (before this time, babies may spontaneously convert)
Caesarean: if ECV unsuccessful/decline/contraindicated
Vaginal breech delivery

377
Q

Important things to consider in vaginal breech delivery

A

Contraindicated in footling breech
‘Hand off the breech’ - do not put traction on baby during delivery as foetal head can extender
Maintain foetal scraum anteriorly by holding pelvis
Manoeuvres to aid delivery:
- Flex foetal knees to enable delivery of legs
- Lovsett’s used to rotate body + deliver shoulders
- Mariceau-Smellie-Veit used to deliver head by flexion

378
Q

UKMEC3 conditions for COCP

A

Disadvantages generally outweigh advantages
>35 years old, smoking <15 cigarettes/day
BMI >35
FHx of thromboembolic disease in first degree relative <45 years
Controlled hypertension
Immobility
Carrier of known gene mutations associated with breast cancer
Current gallbladder disease

379
Q

UKMEC4 conditions for COCP

A

Unacceptable health risk
>35 years old, smoking >15 cigarettes/day
Migraine with aura
History of thromboembolic disease/thrombogenic mutations
History of stroke or ischaemic heart disease
Breastfeeding <6 weeks post-partum
Uncontrolled hypertension
Current breast cancer
Major surgery with prolonged immbolisation
Positive antiphospholipid antibodies e.g. in SLE

380
Q

RIsk factors for VTE in pregnancy

A

Age >35
BMI >30
Parity >/=3
Smoker
Gross varicose veins
Current pre-eclampsia
Immobility
Family history of unprovoked VTE
Low risk thrombophilia
Multiple pregnancy
IVF pregnancy

381
Q

When is prophylaxis of VTE given in pregnancy

A

Three risk fsctors: 28 weeks
Four or more risk factors: first trimester

382
Q

Prophylaxis of VTE in pregnancy

A

Low molecular weight heparin e.g. dalteparin
Continued through antenatal period, and until 6 weeks postnatally
Stopped temporarily during labour, and restarted after delivery
Mechanical prophylaxis given if LMWH contraindicated: intermittent pneumatic compression, or anti-embolic compression stockings

383
Q

Presentation of DVT

A

Unilateral (almost always)
Calf or leg swelling
Dilated superficial veins
Tenderness to calf
Oedema
Colour changes of leg

384
Q

Bedside assessment of DVT

A

Measure calf circumference 10cm below tibial tuberosity
>3cm difference between calves is significant

385
Q

Diagnosis of DVT

A

Doppler ultrasound
Repeated on day 3 + 7 if negative but there is a high index of suspicion

386
Q

Diagnosis of PE in pregnancy

A

Suspected: CXR + ECG
CTPA: given if abnormal CXR, higher risk of breast cancer
VQ perfusion scan: higher risk of childhood cancer for foetus

387
Q

Management of VTE

A

LMWH e.g. dalteparin
Based on weight in booking clinic
Should be started even before diagnosis is confirmed –> continued until 6 weeks postnatally, or three months in total (whichever is longest)
Can switch to oral anticoagulation e.g DOAC or warfarin, adter delivery
Thrombolysis is contraindicated

388
Q

Presentation of obstetric cholestasis

A

Presents later in pregnancy - particularly third trimester
Main symptom = pruritis, particularly affecting palms of hands, and soles of feet
Fatigue
Dark urine
Pale, greasy stools
Jaundice
No rash

389
Q

Investigations for obstetric cholestasis

A

LFTs: abnormal, particularly ALT, AST and GGT (rise in ALP is normal in pregnancy)
Bile acids: raised

390
Q

Risk factors for obstetric cholestasis

A

Hepatitis
Multiple pregnancy
Obstetric cholestasis in previous pregnancy
Gallstones
Family history

391
Q

Managament of obstetric cholestasis

A

Ursodeoxycholic acid - improves LFTs, bile acids, and symptoms
Emollients to soothe skin
Antihistamines can help sleeping
Water-soluble vitamin K given if clotting deranged
Monitor LFTs weekly during pregnancy, and after delivery
Planned delivery after 37 weeks may be considered

392
Q

Symptoms with cervical ectropion

A

Mostly asymptomatic
Increased vaginal discharge, vaginal bleeding or dyspareunia
Postcoital bleeding is common

393
Q

Examination findings for cervical ectropion

A

Well-demarcated border between redder, velvet columnar epithelium extending from os, and pale pink squamous epithelium of ectocervix
Border = transformation zone

394
Q

Risk factors for cervical ectropion

A

Associated with higher oestrogen levels –>
Younger women
COCP use
Pregnancy

395
Q

Management of cervical ectropion

A

Typically resolve with age, stopping of pill, or no longer pregnant
Problematic bleeding –> cauterisation of ectropion using silver nitrate, or cold coagulation during colposcopy

396
Q

Cut offs for treatment of anaemia in pregnancy

A

First trimester <110g/L
Second trimester <105g/L
Postpartum <100g/L

397
Q

Normal thickness of endometrium

A

<5mm