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TO DO WOMENS HEALTH Flashcards

1
Q

ECTOPIC PREGNANCY
What is the epidemiology of ectopics?
What are some risk factors for ectopics?

A

ANATOMICAL FACTORS
- PID
- previous ectopic pregnancy
- tubal surgery
- endometriosis

NON-ANATOMICAL
- IVF
- IUD
- smoking
- POP contraception
- Diethylstilbestrol

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2
Q

ECTOPIC PREGNANCY
What is medical management?
What are the indications?
What indicates that it has worked?

A
  • Single dose IM 50mg/m^2 methotrexate
  • No significant pain, unruptured ectopic <35mm, no heartbeat, serum hCG <1500 (consider up to 5000IU/L) + able to return for follow up
  • hCG levels at days 4 + 7 then weekly, <15% fall = ?another dose
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3
Q

MISCARRIAGE
What is an inevitable miscarriage?

A
  • Miscarriage will occur
  • Heavy PV bleed with clots + crampy abdo pain with OPEN cervical os (1 finger)
  • POC not passed
  • TVS = intrauterine gestation sac, foetus may be alive but miscarriage imminent
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4
Q

MISCARRIAGE
What is the medical management of a miscarriage?
What is the follow up?

A
  • PV/PO synthetic prostaglandin MISOPROSTOL
  • Contact HCP if no bleeding in 24h
  • Urinary beta-hCG 3w after to exclude ectopic or molar
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5
Q

TERMINATING PREGNANCY
What is the medical management of abortion?

A
  • More appropriate in earlier pregnancy, <24w, <10w can be done at home
  • MIFEPRISTONE (anti-progesterone) to halt pregnancy + relax cervix
  • MISOPROSTOL (prostaglandin analogue) 24-48h after for contractions
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6
Q

TERMINATING PREGNANCY
What is done before surgical management of abortion?

A
  • Cervical priming with mifepristone, misoprostol or osmotic dilators (>14w insert into cervix + gradually expand as absorb fluid to open cervical canal)
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7
Q

HYPEREMESIS
What is the diagnostic triad for hyperemesis gravidarum?

A

Triad –
- >5% weight loss compared to before pregnancy
- Dehydration
- Electrolyte imbalance

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8
Q

HYPEREMESIS
What would warrant hospital or EPAU admission?

A
  • Unable to tolerate PO antiemetics or fluids
  • > 5% weight loss compared to before pregnancy
  • Ketones present in dipstick (++ significant)
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9
Q

HYPEREMESIS
What is the inpatient management of hyperemesis gravidarum?

A
  • Monitor U+Es
  • NBM until tolerate PO = IV fluids + anti-emetics
  • Vitamin supplements (incl. thiamine), may need artificial nutrition to prevent Wenicke-Korsakoff
  • Thromboprophylaxis with TED stockings + LMWH
  • Small + frequent meals when eating allowed
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10
Q

HYPEREMESIS
What is the community management of hyperemesis gravidarum?

A
  • 1st line antiemetic = promethazine or cyclizine (anti-histamines)
  • 2nd line = ondansetron (5-HT3 antagonist) or metoclopramide (dopamine antagonist)
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11
Q

ANTENATAL APPTS
What routine care is given at 28w?

A
  • BP, urine dipstick, SFH
  • OGTT if risk factors for GDM
  • Second screen for anaemia (FBC), blood group + rhesus status
  • First dose of anti-D prophylaxis if Rh-ve
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12
Q

ANTENATAL SCREENING
What screening is offered in early pregnancy and when?

A

Combined test (11–13+6w) –
- Nuchal translucency (thickness of back of foetus’ neck on USS)
- Beta-hCG
- Pregnancy associated plasma protein-A (PAPP-A)

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13
Q

ANTENATAL SCREENING
What screening is offered if the mother is too late for the combined test and when?

A

Triple or quadruple test 15–20w but only tests for Down’s syndrome –
- Beta-hCG
- Alpha-fetoprotein
- Oestriol
- Inhibin (quadruple)

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14
Q

ANTENATAL SCREENING
What results indicate higher risk for…
i) beta-HCG?
ii) AFP?
iii) oestriol?
iv) inhibin?

A

i) Higher result
ii) Lower result
iii) Lower result
iv) Higher result

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15
Q

APH
What are some generic investigations for APH?

A
  • Exclude placenta praevia with USS
  • Kleihauer test to confirm transplacental blood loss from foetus>mother
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16
Q

PLACENTA PRAEVIA
What are some risk factors for placenta praevia?

A
  • Embryos more likely to implant on lower segment scar from previous c-section
  • Multiple pregnancy
  • Multiparity
  • Previous praevia
  • Assisted conception
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17
Q

PLACENTAL ABRUPTION
What are the major risk factors for placental abruption?
What are some other risk factors?

A
  • IUGR, pre-eclampsia or pre-existing HTN, maternal smoking + previous abruption
  • Cocaine use, multiple pregnancy or high parity, trauma
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18
Q

PLACENTAL ABRUPTION
What is the general management of placental abruption?

A
  • Mum + foetus stable at <36w then admit + observe carefully, induce after 36w with amniotomy aiming for vaginal delivery, steroids if <34w
  • Anti-D if Rh-ve
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19
Q

ADHERED PLACENTA
What are the different types of morbidly adhered placenta?

A
  • Accreta = placenta invades into superficial myometrium
  • Increta = placenta invades deeper through the myometrium
  • Percreta = placenta invades through myometrium, into nearby organs of abdomen (bladder, bowel)
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20
Q

ADHERED PLACENTA
What are some risk factors for a morbidly adhered placenta?

A
  • Previous c-sections (placenta attaches to site)
  • Myomectomy
  • Surgical TOP
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21
Q

VASA PRAEVIA
What are some risk factors for vasa praevia?

A
  • Placenta praevia
  • Multiple pregnancy
  • IVF pregnancy
  • Bilobed placentas
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22
Q

PRE-ECLAMPSIA
What is the normal physiology of the placenta?

A
  • Spiral arteries dilate + develop into large utero-placental arteries, supplying lots of blood to the endometrium > placenta + foetus
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23
Q

PRE-ECLAMPSIA
What is the pathophysiology of pre-eclampsia?

A
  • Spiral arteries do not remodel + dilate but become fibrous so utero-placental arteries deliver less blood > placental ischaemia
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24
Q

PRE-ECLAMPSIA
What is the result of placental ischaemia?

A
  • Pro-inflammatory protein + thromboplastin release leads to endothelial damage > vasoconstriction, clotting dysfunction + increased vascular permeability
  • Ultimately leads to poor renal perfusion > RAAS activation > HTN, proteinuria ± oedema > pre-eclampsia + eclampsia (if continues)
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25
Q

PRE-ECLAMPSIA

What are the…

i) high risk
ii) moderate risk

factors for pre-eclampsia?

A

i) Pre-existing HTN, previous pre-eclampsia, CKD, autoimmune (SLE, T1DM)
ii) Nulliparity, multiple pregnancy, >10y pregnancy interval, FHx, >40y, BMI >35kg/m^2

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26
Q

PRE-ECLAMPSIA
What are the 2 main causes of symptoms in pre-eclampsia?

A
  • Local areas of vasospasm leading to hypoperfusion
  • Oedema due to increased vascular permeability + hypoproteinaemia
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27
Q

PRE-ECLAMPSIA
What symptoms are caused by local areas of vasospasm and what area is affected?

A

Renal = glomerular damage (low GFR) –
- Oliguria + proteinuria
Retinal –
- Visual disturbances (blurred, flashing lights, scotoma)
Liver = injury + swelling stretches liver capsule –
- RUQ or epigastric pain

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28
Q

PRE-ECLAMPSIA
What symptoms are caused by oedema?

A
  • Face, hands + legs (generalised)
  • SOB + cough (pulmonary)
  • Headaches, confusion + seizures in eclampsia (cerebral)
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29
Q

PRE-ECLAMPSIA
What are the signs of pre-eclampsia?

A
  • Raised BP + proteinuria are hallmarks
  • Rapid weight gain, RUQ tenderness
  • Ankle clonus (brisk reflexes normal in pregnancy but not clonus)
  • Papilloedema if severe
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30
Q

ECLAMPSIA
What is the management of eclampsia?

A

IV magnesium sulfate to prevent + treat seizures –
- Reduces DIC risk as reduced platelet aggregation
- Continue 24h after last seizure or delivery
Treat HTN with labetalol 1st line or nifedipine
Stabilise mum and delivery baby

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31
Q

HELLP
How does HELLP syndrome present?

A

➢ Nausea/vomiting
➢ Hypertension
➢ Brisk tendon reflexes
➢ RUQ/Epigastric pain
➢ General malaise/headache
➢ Oedema/bleeding
➢ Visual problems, jaundice

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32
Q

PRE-ECLAMPSIA
What medical treatment can be given for pre-eclampsia?

A

Treat HTN with –
- PO Labetalol first line (can use IV if severe + inpatient)
- PO nifedipine (used if asthmatic)
- Hydralazine too
- ACEi = CONTRAINDICTAED

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33
Q

PRE-ECLAMPSIA
What is the management of pre-eclampsia during delivery?

A
  • Regular investigations (BP, urinalysis, bloods, CTG, fluid balance chart (restrict if severe)
  • BP control (IV labetalol first line of nifedipine if asthmatic)
  • IV magnesium sulfate prophylaxis during labour + 24h after
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34
Q

IUGR
What are some placental causes of IUGR?

A
  • Abnormal trophoblast invasion (pre-eclampsia, placenta accreta)
  • Infarction, abruption, location (praevia)
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35
Q

IUGR
What are some maternal causes of IUGR?

A
  • Chronic disease (HTN, cardiac, CKD)
  • Substance abuse (cocaine, alcohol) smoking, previous SGA baby
  • Autoimmune
  • Low socioeconomic status
  • > 40
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36
Q

IUGR
What are some foetal causes of IUGR?

A
  • Genetic abnormalities (trisomies 13/18/21, Turner’s)
  • Congenital infections (TORCH)
  • Multiple pregnancy
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37
Q

IUGR
What are some complications of IUGR?

A
  • Hypoglycaemia
  • Risk of necrotising enterocolitis
  • Neonatal jaundice
  • Hypothermia
  • Respiratory issues
  • Long-term sequelae include T2DM, HTN, obesity, behavioural problems, CP
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38
Q

IUGR
What are the investigations for IUGR?

A
  • BP + urine dipstick (?pre-eclampsia)
  • Karyotyping (?foetal)
  • Infection screen, TORCH (?infection)
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39
Q

IUGR
When would you be concerned about IUGR?
What would you do?

A
  • SFH < 10th centile, slow or static growth or crossing centiles
  • Refer for serial growth scans (USS) every 2w, umbilical artery doppler + amniotic fluid volume
  • MCA doppler performed after 32w
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40
Q

MULTIPLE PREGNANCY
What is the management of multiple pregnancies?

A
  • Steroids if <34w
  • Monochorionic/amniotic twins = elective c-section 32-34w
  • Diamniotic twins = 37–38w, vaginal if presenting twin cephalic but may need c-section for second
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41
Q

OLIGOHYDRAMNIOS
What are some causes of oligohydramnios?

A
  • PROM or SROM
  • Renal agenesis (Potter’s syndrome) or non-functional kidneys
  • Placental insufficiency (pre-eclampsia, post-term gestation) as blood redistributed to brain so reduced urine output
  • Genetic anomalies
  • Obstructive uropathy
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42
Q

OLIGOHYDRAMNIOS
What are some complications of oligohydramnios?

A
  • 2nd trimester = poor prognosis due to PPROM leading to premature delivery + pulmonary hypoplasia > resp distress
  • Muscle contractures as amniotic fluid allows foetal to move limbs in utero
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43
Q

POLYHYDRAMNIOS
What are the causes of polyhydramnios?

A
  • Increased foetal urine production (maternal DM), twin-twin transfusion, foetal hydrops
  • Foetal inability to swallow/absorb amniotic fluid (GI tract obstruction e.g. duodenal atresia, foetal neuro/muscular issues)
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44
Q

RHESUS DISEASE
What is the pathophysiology of rhesus disease in the first pregnancy?

A
  • Rh-ve woman exposed to Rh+ve foetal blood, her immune system recognises as foreign + produce antibodies against rhesus D (sensitisation)
  • Usually no issues in 1st pregnancy as IgM produced that cannot cross placenta
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45
Q

RHESUS DISEASE
What is the pathophysiology of rhesus disease in subsequent pregnancies?

A
  • Memory cells produce IgG which can cross placenta so if Rh+ve foetus will attack leading to haemolysis (haemolytic disease of newborn) with jaundice + hydrops fetalis (abnormal accumulation of fluid)
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46
Q

RHESUS DISEASE
What are some investigations for rhesus disease?

A
  • Kleihauer test (check how much foetal blood > mother’s blood after event)
  • All babies born to Rh-ve women should have cord blood at delivery for FBC, blood group + Direct Coombs (antiglobulin) test for antibodies on baby’s RBC
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47
Q

GESTATIONAL DIABETES
What is the pathophysiology of GDM?

A
  • Increased insulin resistance due to placental production of anti-insulin hormones
  • Allows post-prandial glucose peak to be higher for longer to spare glucose for foetus (main source of nutrients)
  • If maternal pancreas cannot increase insulin production to combat this > GDM
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48
Q

GESTATIONAL DIABETES
What are the maternal risks of GDM?

A
  • Pre-eclampsia
  • DKA or hypos
  • UTIs
  • IHD
  • Nephropathy, retinopathy
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49
Q

GESTATIONAL DIABETES
What is the management of GDM?

A
  • Fasting glucose <7 = lifestyle (low GI foods, exercise) > metformin after 1-2w if targets not met
  • Fasting glucose ≥7 = insulin ± metformin
  • Fasting glucose ≥6 + macrosomia or other complications = insulin
  • Glibenclamide if cannot tolerate metformin or decline insulin
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50
Q

VTE IN PREGNANCY
What are the…

i) high
ii) intermediate

risk factors of VTE?

A

i) PMH of VTE, antenatal LMWH requirements, high-risk thrombophilia or low risk + FHx
ii) Smoking, parity >3, age >35, BMI >30, reduced mobility, multiple pregnancy, pre-eclampsia, gross varicose veins, IVF

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51
Q

VTE IN PREGNANCY
How do you manage VTE risk in pregnancy?

A
  • Risk assessment at booking, antenatal admissions + postnatally
  • Antenatal: LMWH from 28w if increased risk or ASAP if high risk
  • Postnatal: LMWH for 10d if increased risk or 6w if high risk
  • TED stockings
  • Low risk Mx = mobilise early, hydration
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52
Q

OBSTETRIC CHOLESTASIS
What is the clinical presentation of obstetric cholestasis?

A
  • Typically later in pregnancy (3rd trimester)
  • Itchy skin (palms of hands + soles of feet) but with NO rash – WORSE at night
  • Jaundice, pale greasy stools + dark urine less common
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53
Q

OBSTETRIC CHOLESTASIS
What are the investigations for obstetric cholestasis?

A
  • Clotting screen (prothrombin time) deranged
  • Abnormal LFTs + raised bile acids (ALT, AST, GGT + bilirubin raised, ALP too but that is normal in pregnancy), monitor LFTs weekly
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54
Q

OBSTETRIC CHOLESTASIS
What is the management of obstetric cholestasis?

A
  • Ursodeoxycolic acid first line to improve LFTs + bile acids
  • Induce labour at 37–38w to reduce stillbirth risk
  • Vitamin K supplementation
  • Emollients (calamine lotion to sooth skin)
  • Antihistamines to help sleep
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55
Q

GROUP B STREP
What is Group B strep (GBS) infection?

A
  • Infection caused by Strep agalactiae
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56
Q

VARICELLA ZOSTER
What is the management of chickenpox exposure in pregnancy?

A
  • Any doubt in immunity, check for varicella zoster IgG
  • ≤20w + not immune = VZIG within 10d
  • > 20w + not immune = VZIG or aciclovir days 7–14 post-exposure
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57
Q

VARICELLA ZOSTER
What is the management of chickenpox infection in pregnancy?

A
  • PO aciclovir if ≥20w + presents within 24h of rash onset
  • <20w then consider
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58
Q

PROM
What are some risk factors for (P)PROM?

A
  • Previous PROM/preterm
  • Smoking
  • Polyhydramnios
  • Amniocentesis
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59
Q

PROM
What are some investigations for PROM?

A
  • Sterile speculum 1st for pooling of amniotic fluid
  • USS may show oligohydramnios if speculum normal
  • Ferning test (cervical secretion on glass slide shows fern-pattern crystals)
  • Test fluid for IGFBP-1 or PAMG-1
  • CTG for foetus (tachycardia is suggestive of infection)
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60
Q

PROM
What is the management of PPROM?

A
  • 1st line = IM corticosteroids if foetus <34w
  • Prophylactic PO erythromycin given to prevent chorioamnionitis for 10d or until labour is established if within 10d
  • Consider induction at 34w (trade off)
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61
Q

STAGES OF LABOUR
What are 7 important hormones in labour?

A
  • Prostaglandins
  • Oxytocin
  • Oestrogen
  • Beta-endorphins
  • Adrenaline
  • Prolactin
  • Relaxin
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62
Q

STAGES OF LABOUR
What is the first stage of labour?
How is it further divided?

A
  • From onset of labour (true contractions) until the cervix is fully dilated
  • Latent phase = from 0–3cm dilation
  • Active phase = from 3–10cm
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63
Q

STAGES OF LABOUR
What is the second stage of labour?
How is it further divided?

A
  • From full dilation to delivery of the foetus
  • Passive stage: complete dilation but no pushing (often 1 hour)
  • Active stage: maternal pushing until delivery
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64
Q

STAGES OF LABOUR
What is considered a delay in the active second stage of labour?
What does success depend on?

A
  • > 2h in nulliparous, 1h in multiparous
  • 3Ps (power, passenger + passage [?Psyche of mum])
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65
Q

STAGES OF LABOUR
What are the parts of the APGAR score?

A

Activity – absent 0, flexed arms + legs 1, active 2
Pulse – absent 0, <100bpm 1, >100bpm 2
Grimace – floppy 0, minimal response to stimulation 1, prompt response to stimulation 2
Appearance – blue 0, blue extremities 1, pink 2
Respiration – absent 0, slow + irregular 1, vigorous cry 2

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66
Q

STAGES OF LABOUR
What are the 6 cardinal movements of labour?

A
  • Engagement + descent
  • Flexion
  • Internal rotation
  • Extension (crowning)
  • Restitution/external rotation
  • Expulsion
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67
Q

STAGES OF LABOUR
What position is the foetal head during engagement and descent?

A
  • Occiput transverse
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68
Q

FAILURE TO PROGRESS
What may be calculated when considering inducing labour?
What does it calculate?

A
  • Bishop score = used to calculate how likely spontaneous labour is to occur
  • Score <5 = unripe cervix (less likely for induction success)
  • Score >9 = favourable cervix ready for labour or induction
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69
Q

FAILURE TO PROGRESS
What are the components of the Bishop score?

A
  • Cervical dilation – <1cm (0), 1-2 (1), 3-4 (2), >5cm (3)
  • Cervical consistency – firm (0), intermediate (1), soft (2)
  • Cervical effacement –<30% (0), 40-50 (1), 60-70 (2), 80% (3)
  • Cervical position – posterior (0), intermediate (1), anterior (2)
  • Foetal station – –3 (0), -2 (1), -1/0 (2), ≥1 (3)
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70
Q

FAILURE TO PROGRESS
What are some methods of inducing labour?

A
  • Membrane sweep
  • Prostaglandin E2 (PGE2) pessary or gel like dinoprostone
  • Cervical ripening balloon (gently inflates + dilates cervix)
  • Amniotomy if not ruptured already
  • Oxytocin analogue (syntocinon) infusion to cause uterine contractions
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71
Q

FAILURE TO PROGRESS
What are some indications and contraindications for inducing labour?

A
  • PROM, IUGR, pre-eclampsia, obstetric cholestasis
  • Severe degree of placenta praevia, transverse foetal lie, severe cephalopelvic disproportion, low Bishop score
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72
Q

FAILURE TO PROGRESS
In terms of ‘passenger’ in failure to progress, what is important about position?

A
  • Refers to foetal head position on VE
  • Anterior/posterior fontanelles as landmarks, OA ideal
  • If OP at delivery means head is at posterior quadrant of pelvis requiring greater rotation which can prolong labour
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73
Q

FAILURE TO PROGRESS
How would you manage failure to progress in the first stage of labour?

A
  • PGE2 if low bishop score as if not cannot induce
  • Oxytocin infusion ± amniotomy (if membranes not ruptured) > reassess in 2h
  • CTG with foetal blood sample if concerns, consider c-section if doesn’t help
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74
Q

FAILURE TO PROGRESS
How would you manage failure to progress in the third stage of labour?
What are the indications for management?

A
  • IM oxytocin to cause uterus contraction to expel placenta
  • Cord clamp + careful cord traction to guide placenta out
  • Haemorrhage or >60m delay in physiological management (delay in active Mx is >30m)
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75
Q

BREECH
What are some causes/risk factors for breech presentation?

A
  • Idiopathic
  • Prematurity as baby may not have turned itself yet
  • Previous breech
  • Uterine abnormalities (bicornuate uterus), fibroids
  • Placenta praevia
  • Foetal abnormalities (CNS malformation
  • Multiple pregnancy
  • Poly/oligohydramnios
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76
Q

BREECH
What are the 3 types of breech presentation?

A
  • Extended (Frank) = most common, hips flexed, both legs extended with feet by head, buttocks presenting
  • Flexed (Complete) = hips + knees flexed so buttocks + feet presenting (Cannonballing)
  • Footling = one leg flexed, one extended, foot hanging through cervix
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77
Q

CTG
What are the indications for a continuous cardiotocography (CTG)?

A
  • During labour for every woman
  • High risk pregnancies
  • Pyrexia (?chorioamnionitis)
  • Severe HTN ≥160/110
  • Oxytocin use
  • Fresh bleeding
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78
Q

CTG
How do you interpret a CTG?

A

Dr C Bravado –
- Dr = define risk (high risk = continuous
- C = contractions (bottom trace shows frequency)
- Bra = baseline rate
- V = variability
- A = accelerations
- D = decelerations
- O = overall assessment

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79
Q

CORD PROLAPSE
What are some risk factors for cord prolapse?

A
  • Prematurity
  • Polyhydramnios
  • Long umbilical cord
  • Malpresentation (Footling breech + transverse lie)
  • Multiparity + multiple pregnancy
  • Placenta praevia
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80
Q

CORD PROLAPSE
What is the management of cord prolapse?

A
  • 999/emergency buzzer, neonatal team
  • Fill bladder with 500ml warmed saline via catheter (elevate presenting foetal part + lift off cord)
  • Left lateral position with head down or knee-chest position
  • Presenting part pushed back into uterus to prevent compression
  • Avoid handling cord > vasospasm
  • Tocolytics like terbutaline (SABA) to abolish contractions if delivery not imminently available
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81
Q

SHOULDER DYSTOCIA
What are some risk factors for shoulder dystocia?

A
  • Macrosomia
  • Maternal DM
  • High maternal BMI
  • Cephalopelvic disproportion
  • Post-maturity
  • Previous shoulder dystocia
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82
Q

SHOULDER DYSTOCIA
Explain what is the result of…

i) erb’s palsy?
ii) clavicle fracture?

A

i) Injury of C5/6 nerves causing paralysis of arm, looks limp, waiters tip position
ii) Painful movements, shoulder asymmetry

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83
Q

SHOULDER DYSTOCIA
What is the management of shoulder dystocia?

A

HELPERR[R] –
- Help (call with emergency buzzer, obs, neonates)
- Evaluate for episiotomy (enlarge opening)
- Legs = McRobert’s
- Pressure = suprapubic
- Enter = pelvis for rotation
- Remove = posterior arm
- Replace = head in vagina + deliver by section (Zavanelli)

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84
Q

INSTRUMENTAL DELIVERY
What are the main risks of ventouse delivery?

A
  • Cephalohaematoma = collection of blood between periosteum + skull from damaged blood vessels, does not cross suture lines, presents hours after
  • Caput Succedaneum = Crosses Sutures, diffuse oedema outside periosteum due to pressure to a specific area of scalp, resolve in few days, conehead present at birth
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85
Q

INSTRUMENTAL DELIVERY
What are some maternal consequences of instrumental delivery?

A
  • Infection (co-amox stat)
  • PPH
  • Episiotomy
  • Tears
  • Incontinence
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86
Q

C-SECTION
What are the different categories of c-section?

A
  • 1 = immediate threat to life of mother/baby. Decision>delivery time = 30m
  • 2 = not imminent threat to life but c-section required urgently due to compromise. Decision>Delivery time = 75m
  • 3 = c-section required but both stable
  • 4 = elective section
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87
Q

PERINEAL TEARS
What is the classification of perineal tears?

A
  • 1st degree = limited to superficial skin of perineum
  • 2nd degree = above PLUS perineal muscles (includes episiotomy)
  • 3rd degree = above PLUS anal sphincter involvement
  • 4th degree = above PLUS injury to rectal mucosa
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88
Q

PERINEAL TEARS
How are third degree tears further classified?

A
  • 3A = <50% of external anal sphincter thickness torn
  • 3B = >50% of EAS thickness torn
  • 3C = EAS + internal anal sphincter torn
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89
Q

PPH
What is a primary postpartum haemorrhage (PPH)?

A

Primary = loss of >500ml blood in the first 24h after delivery
- Minor = 500–1000ml estimated blood loss
- Major = >1000ml, clinically in shock

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90
Q

PPH
What are the primary causes of PPH?

A

Primary (4Ts)–
- Tone (uterine atony = most common)
- Trauma (perineal tear)
- Tissue (retained products)
- Thrombin (clotting issue e.g. DIC in pre-eclampsia)

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91
Q

PPH
What are some preventative measures to reduce risk and consequences of PPH?

A
  • Treat anaemia during antenatal period
  • Empty bladder (?catheter) as full bladder reduces uterine contractions
  • Active Mx of third stage (IM oxytocin)
  • IV TXA during c-section in third stage of labour if high risk
92
Q

PPH
What is the role of medical management in PPH?
What is the medical management of PPH?

A
  • All stimulate uterine contractions
  • IV syntocinon
  • IV/IM ergometrine, C/I in HTN as vasoconstrictor (can combine with syntocinon as syntometrine)
  • IM carboprost, caution in asthma (prostaglandin analogue)
  • Sublingual misoprostol (prostaglandin analogue)
93
Q

PPH
After failed medical management, what is the surgical management of PPH?

A
  • Intrauterine balloon tamponade (1st line in uterine atony)
  • B-lynch sutures (suture around uterus to compress it)
  • Internal iliac/uterine artery ligation (reduces blood flow to stop bleeding)
  • Hysterectomy as last resort (may save life)
94
Q

HYPEREMESIS
What are some associations of hyperemesis gravidarum?

A
  • nulliparity,
  • hyperthyroid,
  • obesity,
  • decreased in smokers
95
Q

HYPEREMESIS
How is severity assessed?

A

Pregnancy-Unique Quantification of Emesis (PUQE) –
- <7 mild,
- 7-12 mod,
- >12 severe

96
Q

STAGES OF LABOUR
What is the role of oxytocin in labour?

A

Produced by hypothalamus, secreted by post. pituitary, surge at labour inhibits progesterone to prepare smooth muscle for uterine contractions, milk ejection reflex postpartum

97
Q

PPH
What is a secondary postpartum haemorrhage (PPH)?

A

Secondary = excessive blood loss from genital tract between 24h–12w after delivery (can result in Sheehan’s syndrome)

98
Q

HELLP
what other condition is HELLP associated with?

A
  • 10% have antiphospholipid syndrome
99
Q

HELLP
what are the risk factors for HELLP?

A

➢ White ethnicity
➢ Maternal age >35 yrs.
➢ Obesity
➢ Chronic hypertension
➢ DM
➢ Autoimmune disorders
➢ Abnormal placentation and multiple gestation
➢ Previous pregnancy with preeclampsia

100
Q

HELLP
what is the management for HELLP?

A

➢ Seizure prophylaxis (magnesium sulfate), IV dexamethasone, labetalol. IM beclametasone
when patient <36wks
➢ Delivery is definitive treatment (should be done when patient is 37+ wks)

101
Q

FOETAL HYDROPS
what is the pathophysiology?

A

an imbalance of interstitial fluid production and inadequate lymphatic return. This can result from congestive heart failure, obstructed lymphatic flow, or decreased plasma osmotic pressure.

102
Q

FOETAL HYDROPS
what are the causes of immune foetal hydrops?

A

results from blood group incompatibility between the mother and the fetus causing fetal anaemia.
THIS IS RHESUS DISEASE OF THE NEWBORN**

103
Q

FOETAL HYDROPS
what are the causes of non-immune foetal hydrops

A
  • severe anaemia (parvovirus B19, thalassaemia, G6PD)
  • cardiac abnormalities
  • chromosomal abnormalities (trisomies 13, 18 and 21)
  • genetic conditions
  • other infections (toxoplasmosis, rubella, CMV, varicella)
  • structural abnormalities (CCAM, diaphragmatic hernia)
  • twin-to-twin transfusion syndrome
  • chorioangioma
104
Q

FOETAL HYDROPS
what is the management?

A

depends on the cause
- anaemia = in-utero blood transfusion
- pleural effusions/CCAM = shunt
- twin-to-twin transfusion syndrome = laser photocoagulation of placental anastomoses
- cardiac arrhythmias = maternal digoxin + flecanide

105
Q

UTEROPLACENTAL INSUFFICIENCY
what are the causes of uteroplacental insufficiency?

A

➢Abnormal trophoblast invasion:
▪ Pre-eclampsia
▪ Placenta accreta
➢ Abruption
➢ Infarction
➢ Placenta previa
➢ Tumor: chorioangiomas
➢ Abnormal umbilical cord or cord insertion (i.e., two vessel cord)
➢ Maternal diabetes
➢ Maternal hypertension
➢ Anemia
➢ Smoking
➢ Drug abuse (cocaine, heroin, methamphetamine)
➢ Antiphospholipid syndrome
➢ Renal disease
➢ Advanced age

106
Q

UTEROPLACENTAL INSUFFICIENCY
what is the presentation?

A

➢ Depending on the cause
➢ Mother may notice uterus is smaller than previous pregnancies
➢ Fetus may be moving less than expected
➢ IUGR
➢ Vaginal bleeding or preterm labor contractions (i.e., during placental abruption)

107
Q

PUERPERAL INFECTION
what is it defined as?

A

Temperature of above 38 degrees Celsius in the first 14 days following delivery.

108
Q

PUERPERAL INFECTION
what is the management?

A

➢ Supportive (analgesics/NSAIDS, wound care, ice packs…)
➢ Antibiotics (for endometritis – IV clindamycin and gentamicin until >24hrs afebrile)
➢ Surgical (drain abscess, secondary repair of wound, drainage of hematomas…)

109
Q

OBSTRUCTED LABOUR
What are the different types of causes of obstructed labour?

A
  • Power (most common)
  • Passage
  • Passenger
  • Psyche (maternal exhaustion in second stage)
110
Q

MISCARRIAGE
What is the management of antiphospholipid syndrome?

A

Low dose aspirin + LMWH

111
Q

CHORIONIC VILLUS SAMPLING
when is chorionic villus sampling performed?

A

Usually between 10-13 weeks

112
Q

AMNIOCENTESIS
When is amniocentesis performed?

A

from 15 weeks onwards

113
Q

CHLAMYDIA IN PREGNANCY
what is the management?

A
  • azithromycin 1g OD followed by 500mg orally OD for 2 days
  • erythromycin 500mg QD for 7 days
  • amoxicillin 500mg TD for 7 days
114
Q

GONORRHOEA IN PREGNANCY
what are the risks?

A
  • miscarriage
  • premature birth
  • low birth weight
  • PROM
  • chorioamnionitis
  • eye infection in newborn
115
Q

GONORRHOEA IN PREGNANCY?
what is the management?

A

500mg ceftriaxone IM single dose

116
Q

SYPHILIS IN PREGNANCY
what is the management?

A

penicillin

117
Q

TRICH VAGINALIS IN PREGNANCY
what is the management?

A

metronidazole

118
Q

UTIs IN PREGNANCY
what are the treatments?

A
  • Oral antibiotics
    - Asymptomatic bacteriuria: 3 days
    - Cystitis 7 days
  • nitrofurantoin (avoid in 3rd trimester)
  • amoxicillin (only once sensitivities known)
  • cefalexin
119
Q

UTIs IN PREGNANCY
what is the management of pyelonephritis?

A

antibiotics (IV) for 10-14 days
- Pyelonephritis needs IV antibiotics until pyrexia settles and vomiting stops. IV fluids and antipyretics too.

120
Q

UTIs IN PREGNANCY
what are the antenatal risk factors for UTIs?

A
  • previous infection
  • renal stones
  • diabetes mellitus
  • immunosuppression
  • polycystic kidneys
  • congenital abnormalites of renal tract
  • neuropathic bladder
121
Q

CEPHALOPELVIC DISPROPORTION
what can increase the risk?

A
  • flat (platypelloid) pelvic opening
  • heart-shaped (android) pelvis
122
Q

MISCARRIAGE
what is the management of a threatened miscarriage?

A

vaginal progesterone 400mg BD

offered to women with confirmed intrauterine pregnancy, if they have vaginal bleeding and previous miscarriage

if foetal heartbeat is confirmed, continue progesterone until 16 weeks

123
Q

ANAEMIA + PREGNANCY
what are the cut offs for the normal ranges of haemoglobin during pregnancy?

A

1st trimester = <110g/L
2nd/3rd trimester = <105g/L
Postpartum = <100g/L

124
Q

PREMATURE LABOUR
how can premature labour be prevented?

A
  • vaginal progesterone gel/pessary (if cervical length <25mm on vaginal USS at 16-24 weeks)
  • cervical cerclage (if cervical length <25mm on vaginal USS at 16-24 weeks and have had previous premature birth or cervical trauma)
  • rescue cervical cerclage offered at 16-27+6 weeks when there is cervical dilatation without ROM
125
Q

PREMATURE LABOUR
what medications can stop uterine contractions?
when are they used?

A
  • nifedipine or atosiban
  • used between 24-33+6 weeks
  • used to delay delivery and buy time for further foetal development, administration of steroids or transfer to a more specialist unit
  • only used as a short term measure (<48 hours)
126
Q

FIBROIDS
What are some risk factors for fibroids?

A
  • Afro-Caribbean
  • Obesity
  • Early menarche
  • FHx
  • Increasing age (until menopause)
127
Q

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

A
  • Tranexamic acid (antifibrinolytic) taken during bleeding to reduce it
  • Mefenamic acid (NSAID) to reduce bleeding + pain
128
Q

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

A
  • Mirena coil is 1st line (fibroids <3cm with no uterus distortion)
  • 2nd = COCP triphasing (back-to-back for 3m then break)
  • Cyclical oral progestogens
  • Norethisterone 5mg TDS can be used short-term to rapidly stop menorrhagia from 3d before period until bleeding acceptable
129
Q

FIBROIDS
What is the management of fibroids >3cm?

A
  • Same medical Mx but surgery offered too
  • GnRH agonists (goserelin) can be given to shrink fibroids by inducing menopausal state (reduced oestrogen) in short-term (can demineralise bone) for surgery
  • Selective progesterone receptor modulators (SPRMS) like ulipristal acetate can be used instead to avoid SEs
130
Q

ADENOMYOSIS
What are the investigations for adenomyosis?

A
  • Bimanual exam = bulky + tender uterus, ‘BOGGY’
  • TVS is 1st line investigation
  • Gold standard - histological examination of uterus after hysterectomy (not always suitable though)
131
Q

ADENOMYOSIS
What is the initial management of adenomyosis?

A

if pt does NOT want contraception
- anti-fibrinolytic = TRANEXAMIC ACID (when there is no associated pain)
- NSAID = MEFANAMIC ACID (when there is associated pain)

if pt does want contraception
- 1st line = mirena coil
- COCP
- cyclical oral progestogens

other options (considered by specialist)
- GnRH analogues
- endometrial ablation
- uterine artery embolism
- hysterectomy

132
Q

ENDOMETRIOSIS
What are some risk factors for endometriosis?

A
  • Early menarche,
  • late menopause,
  • obstruction to vaginal outflow (imperforate hymen)
133
Q

ENDOMETRIOSIS
What is the initial management of endometriosis?

A
  • NSAIDs ± paracetamol first line for Sx relief
  • COCP triphasing (can’t take for longer as if not irregular bleeding
  • POP like medroxyprogesterone acetate
  • GnRH analogues to “induce” menopause, reversible, quicker than triphasing but need HRT + only short-term as risk of osteoporosis
134
Q

PCOS
How does insulin resistance contribute to PCOS?

A
  • Insulin resistance = pancreas produces more insulin
  • Insulin mimics action of insulin-like growth factor 1 which augments androgen production by theca cells in response to LH
  • Higher insulin = higher androgens (testosterone)
135
Q

PCOS
How does high insulin levels contribute to PCOS?

A
  • Insulin suppresses sex hormone-binding globulin (SHBG) produced by liver which normally binds to androgens + suppresses their function further promoting hyperandrogenism
  • Also contribute to halting development of follicles in ovaries > anovulation + multiple partially developed follicles (polycystic ovaries)
136
Q

PCOS
What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism
  • Insulin resistance
  • Oligo or amenorrhoea + sub/infertility
137
Q

PCOS
How does insulin resistance present?

A
  • Obesity, acanthosis nigricans (thickened, rough skin often axilla + elbows with velvety texture), psychological Sx
138
Q

PCOS
What diagnostic criteria is used in PCOS?

A

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

139
Q

PCOS
What hormone tests may be used in PCOS?

A
  • Testosterone (raised)
  • SHBG (low)
  • LH (raised) + raised LH:FSH ratio (LH>FSH)
  • Prolactin (normal), TFTs (exclude causes)
140
Q

PCOS
What other investigation may be useful at indicating PCOS?

A

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

141
Q

PCOS
What are some associations and complications of PCOS?

A
  • DM, CVD + hypercholesterolaemia
  • Obstructive sleep apnoea, MH issues, sexual problems
  • Endometrial hyperplasia or cancer
142
Q

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

A
  • Obesity, DM, insulin resistance, amenorrhoea
  • Mirena coil for continuous endometrial protection
  • Induce withdrawal bleed AT LEAST every 3m with COCP or cyclical progesterones medroxyprogesterone 10mg 14d)
143
Q

PCOS
How is infertility managed in PCOS?

A
  • Weight loss initial step to restore regular ovulation
  • Clomiphene to induce ovulation
  • Metformin may help (+ helps insulin resistance)
  • Laparoscopic ovarian drilling or IVF last resort
144
Q

CERVICAL CANCER
What genes may be implicated in cervical cancer?

A
  • P53 + pRb are tumour suppressor genes
  • HPV produces two oncoproteins (E6 + E7)
  • E6 inhibits P53, E7 inhibits pRB
145
Q

CERVICAL CANCER
How is cervical cancer staged?

A

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

146
Q

CERVICAL CANCER
What is the cervical cancer screening?

A
  • Sexually active women 25–64 (triennially 25–50, 5y 50–64) smear test
  • Exceptions = HIV pts screened annually, women with previous CIN may require additional tests
147
Q

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

A
  • Cervical intra-epithelial neoplasia (CIN)
  • CIN I = mild, affects 1/3 thickness of epithelial layer, likely to return to normal without Tx
  • CIN II = mod, affects 2/3 thickness of epithelial layer, likely to progress to cancer without Tx
  • CIN III or cervical carcinoma in situ = severe, v likely to progress to cancer without Tx
148
Q

OVARIAN CANCER
What are the 4 types of ovarian cancer?

A
  • Epithelial cell tumours (85–90%)
  • Germ cell tumours (common in women <35)
  • Sex cord-stromal tumours (rare)
  • Metastatic tumours
149
Q

OVARIAN CANCER
What are some types of epithelial cell tumours?

A
  • Serous carcinoma (#1)
  • Endometrioid, clear cell, mucinous + undifferentiated tumours too
150
Q

OVARIAN CANCER
What are sex-cord stromal tumours?

A
  • Arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles)
  • Sertoli-Leydig + granulosa cell tumours
151
Q

OVARIAN CANCER
What are metastatic tumours?

A
  • Secondary tumours
  • Krukenberg = metastasis in ovary, usually from GI (stomach) > CLASSIC “SIGNET-RING” CELLS ON HISTOLOGY
152
Q

OVARIAN CANCER
What are some risk factors of ovarian cancer?

A

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

153
Q

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

A
  • COCP
  • Early menopause
  • Breast feeding
  • Childbearing
154
Q

OVARIAN CANCER
How is the risk of malignancy index calculated?

A
  • Menopausal status = 1 (pre) or 3 (post)
  • Pelvic USS findings = 1 (1 feature) or 3 (>1 feature)
  • CA-125 levels IU/mL as marker for epithelial cell ovarian cancer
155
Q

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

A
  • Endometriosis
  • Fibroids + adenomyosis
  • Pelvic infection
  • Pregnancy
  • Benign cysts
156
Q

OVARIAN CANCER
What staging is used in ovarian cancer?

A

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

157
Q

OVARIAN CYST
What are the 4 types of ovarian cysts?

A
  • Functional (physiological)
  • Benign epithelial neoplasms
  • Benign germ cell neoplasms
  • Benign sex-cord stromal neoplasms
158
Q

OVARIAN CYST
What are the three types of functional cysts?

A
  • Follicular (most common)
  • Corpus luteum
  • Theca lutein
159
Q

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

A
  • Corpus luteum fails to breakdown, may fill with fluid or blood
  • May burst causing intraperitoneal bleeding
  • Early pregnancy
160
Q

OVARIAN CYST
What are theca lutein cysts?
Association?

A
  • Stimulates growth of follicular theca cells so usually bilateral as resting follicles on both sides
  • Overstimulation of hCG (multiple + molar pregnancy as hCG v high)
161
Q

OVARIAN CYST
What are some features of neoplastic cysts?

A
  • Often complex
  • > 10cm
  • Irregular borders
  • Internal septations appearing multi-locular
  • Heterogenous fluid
162
Q

OVARIAN CYST
What are the 2 benign epithelial neoplasms?

A
  • Serous cystadenoma (most common epithelial tumour)
  • Mucinous cystadenoma
163
Q

OVARIAN CYST
How does serous cystadenoma present?

A
  • May be bilateral, filled with watery fluid, 30–50y
164
Q

OVARIAN CYST
How does mucinous cystadenoma present?

A
  • Often very large + contain mucus-like fluid
  • Pseudomyxoma peritonei where abdo cavity fills with gelatinous mucin secretions if rupture
  • 30–40y
165
Q

OVARIAN CYST
What are benign germ cell neoplasms?

A
  • Dermoid cysts or teratomas
  • Common in women <35
  • May contain various tissue types (skin, teeth, hair + bone)
  • Can be bilateral, associated with ovarian torsion as heavy
166
Q

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

A
  • Fibromas (small, solid benign fibrous tissue tumour)
  • Associated with Meig’s syndrome
167
Q

OVARIAN CYST
What are some risk factors of ovarian cysts?

A
  • Obesity, tamoxifen, early menarche, infertility
  • Dermoid cysts = most common in young women, can run in families
  • Epithelial cysts = most common in post-menopausal (?malignant)
168
Q

OVARIAN CYST
What investigations should be done for ovarian cysts?

A
  • Beta-hCG to exclude uterine or ectopic
  • FBC for infection or haemorrhage
  • CA-125 if >40
  • Germ cell tumour markers if <40 with complex ovarian mass
  • Imaging (TVS or MRI abdo if larger mass)
  • Diagnostic laparoscopy (gold standard in ruptured cyst)
  • May need USS guided aspiration + cytology to confirm benign
169
Q

OVARIAN CYST
What are the germ cell tumour markers?

A
  • Lactate dehydrogenase
  • Alpha-fetoprotein
  • Human chorionic gonadotropin
170
Q

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

A
  • Small <5cm = likely to resolve within 3 cycles, no follow up
  • Mod 5–7cm = routine gynae referral + yearly USS
  • Large >7cm = ?MRI + surgical evaluation
171
Q

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

A
  • Risk of malignancy index calculation
  • Simple cysts <5cm + normal CA-125 = monitor with 4–6m USS
  • Complex cyst or raised CA-125 = 2ww gynae oncology referral
172
Q

ENDOMETRIAL CANCER
What are some risk factors for endometrial cancer?

A

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

173
Q

ENDOMETRIAL CANCER
What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking (Seem to have anti-oestrogenic effect)
174
Q

ENDOMETRIAL CANCER
What is the staging for endometrial cancer?

A

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

175
Q

ENDOMETRIAL POLYP
What are some risk factors of endometrial polyps?

A
  • Being peri or post-menopausal
  • HTN
  • Obesity
  • Tamoxifen
176
Q

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

A
  • Rare compared to other cancers
  • Squamous cell carcinomas (90%), malignant melanoma less common
177
Q

VULVAL CANCER
What are some risk factors for vulval cancer?

A
  • Vulval intraepithelial neoplasia (VIN) due to HPV in younger women
  • Lichen sclerosus in older women
178
Q

VULVAL CANCER
How is vulval cancer staged?

A

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

179
Q

VULVAL CANCER
What is the management of VIN?

A
  • Biopsy to Dx
  • Watch + wait with close follow up
  • Wide local excision to surgically remove lesion
  • Imiquimod cream or laser ablation
180
Q

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

A
  • 90% squamous
181
Q

MENOPAUSE
What are the peri-menopausal symptoms?

A
  • Vasomotor = hot flushes, night sweats, impact on QOL
  • General = mood swings, decreased libido, vaginal dryness, headache, dry skin, loss of energy, joint aches, muscles pains, irregular periods
182
Q

MENOPAUSE
Why does urogenital atrophy occur?

A
  • Urogenital tract has oestrogen receptors + continual stimulation keep it strong + supple
183
Q

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

A
  • UKMEC1 = barrier, IUS/IUD, POP, long-acting progesterone (<45), sterilisation
  • UKMEC2 = COCP after 40 used until 50, try ones with levonorgestrel or norethisterone as lower VTE risk
  • They don’t but may mask Sx
184
Q

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

A
  • HRT first-line for vaso-motor Sx as most effective
  • Clonidine (alpha adrenergic receptor agonist) second line with low-dose antidepressants like venlafaxine (not C/I in breast cancer Tx) or fluoxetine
  • CBT
  • Vaginal oestrogen cream/tablets + moisturisers for dryness
185
Q

MENOPAUSE
What is the mechanism of action of clonidine?

A
  • Alpha-adrenergic receptor agonist
186
Q

HRT
What are some benefits of HRT?

A
  • Improved Sx control
  • Improved QOL
  • Reduced risk of osteoporosis
187
Q

HRT
What are some risks with HRT?

A
  • Increased risk of breast cancer by adding progesterone
  • Increased risk of endometrial cancer by oestrogen alone
  • Increased risk of VTE
  • Increased risk of stroke + IHD
188
Q

HRT
What are some contraindications to HRT?

A
  • Undiagnosed PV bleeding
  • Current or past breast cancer
  • Any oestrogen sensitive cancer (endometrial)
189
Q

HRT
What HRT would you give to…

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

A

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

190
Q

HRT
What are the side effects associated with oestrogen?

A
  • Nausea,
  • bloating,
  • headaches,
  • breast swelling or tenderness,
  • leg cramps
191
Q

ATROPHIC VAGINITIS
What is the pathophysiology of atrophic vaginitis?

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

ATROPHIC VAGINITIS
What are some risk factors for atrophic vaginitis?

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

URINARY INCONTINENCE
What is the physiology of micturition?

A
  • Detrusor = smooth muscle, transitional epithelium normally only contracts during micturition = sacral parasympathetic innervation from S2-4
  • M2+3 muscarinic receptors with ACh
  • Sympathetic nerve fibres from T11-L2 maintain relaxation of bladder for storage
194
Q

URINARY INCONTINENCE
What causes urge incontinence/OAB?

A
  • Overactivity + involuntary contractions of the detrusor muscle
195
Q

URINARY INCONTINENCE
What are some causes of overflow incontinence?

A
  • Anticholinergics
  • Fibroids
  • Pelvic tumours
  • BPH (men)
  • Neuro (damage, MS, diabetic neuropathy, spinal cord injuries)
196
Q

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

A
  • 1st line = bladder retraining (6w gradually increasing time between voiding)
  • 1st line drugs = anti-muscarinics (oxybutynin, tolterodine, darifenacin)
  • Mirabegron (beta-3-adrenergic agonist) if anti-muscarinics not tolerated
  • specialist referral for botox injections + surgery
197
Q

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

A
  • Parasympathetic so Pissing = decreases need to urinate + spasms
198
Q

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

A
  • Sympathetic so Storage = relaxes detrusor + increases bladder capacity
199
Q

URINARY INCONTINENCE
What are last resort options for urge incontinence?

A
  • Augmentation cystoplasty with bowel tissue
  • Bypass (urostomy)
  • Botox can paralyse detrusor + block ACh release
200
Q

URINARY INCONTINENCE
What are the surgical interventions for stress incontinence?

A
  • Colposuspension
  • Tension free vaginal tape (TVT)
  • Autologous sling procedures (TVT but strip of fascia from abdo wall)
201
Q

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

A
  • Age
  • BMI
  • Multiparity (vaginal)
  • Spina bifida
  • Pelvic surgery
  • Menopause
202
Q

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

A
  • Sim’s speculum (U-shaped) to show if something is there
  • May have urodynamics, USS or MRI
203
Q

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

A
  • Conservative = pelvic floor exercises, weight loss + diet changes
  • Vaginal pessary = ring (preferred as can have sex), shelf or Gellhorn
  • Surgery (symptomatic or severe like outside vagina, ulcerated, failed Mx)
204
Q

DYSMENORRHOEA
What is the management of primary dysmenorrhoea?

A
  • NSAIDs like mefenamic acid during menstruation
  • COCP second line
205
Q

ASHERMAN’S SYNDROME
What causes Asherman’s syndrome?

A
  • Pregnancy-related dilatation + curettage procedures
  • After uterine surgery
  • Pelvic infection like endometritis
206
Q

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

A
  • Secondary amenorrhoea
  • Infertility
  • Significantly lighter periods
  • Dysmenorrhoea
207
Q

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

A
  • Hysterosalpingography = contrast injected into uterus + XR
  • Sonohysterography = uterus filled with fluid + pelvic USS
  • Hysteroscopy gold standard + can dissect adhesions (recurrence after common)
208
Q

ENDOMETRIOSIS
What are some protective factors?

A

Multiparity + COCP

209
Q

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

A
  • Most common cancer in women <35
  • Squamous cell carcinoma 80%, then adenocarcinoma (small cell rare)
210
Q

VAGINAL CANCER
What causes it?

A

HPV or metastatic spread from cervix or vulva

211
Q

HRT
What are the side effects associated with progesterone?

A

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

212
Q

HYDATIDIFORM MOLE
What is a complete mole?

A
  • Diploid trophoblast cells
  • Empty egg + sperm that duplicates DNA (all genetic material comes from father)
  • 46 chromosomes
  • No foetal tissue
213
Q

HYDATIDIFORM MOLE
What is a partial mole?

A
  • Triploid (69XXX, 69XXY) trophoblast cells
  • 2 sperm fertilise 1 egg
  • Some recognisable foetal tissue
214
Q

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

A
  • When a complete mole invades the myometrium
  • Metaplastic potential to evolve into a choriocarcinoma
215
Q

HYDATIDIFORM MOLE
What are some risk factors for hydatidiform mole?

A
  • Extremes of reproductive age
  • Previous molar pregnancy
  • Multiple pregnancies
  • Asian women
  • OCP
216
Q

PELVIC INFLAMMATORY DISEASE
What are the STI causes of PID?

A
  • N. gonorrhoea (tends to be more severe),
  • chlamydia trachomatis (most common),
  • Mycoplasma genitalium
217
Q

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

A
  • Pus cells on swabs from vagina or endocervix
  • Absence is useful to exclude PID
218
Q

PELVIC INFLAMMATORY DISEASE
What is the management of PID?

A
  • 1g stat IM ceftriaxone (gonorrhoea)
  • 100mg BD doxycycline for 14d (chlamydia + MG)
  • Metronidazole 400mg BD for 14d (Gardnerella)
  • GUM referral for specialist Mx + contact tracing
  • Hospital admission for IV Abx if signs of sepsis or pregnant
  • Pelvic abscess > drainage
219
Q

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

A
  • Post-partum (retained tissue),
  • uterine instrumentation (hysteroscopy, IUCD),
  • descended from other organs (appendicitis)
220
Q

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

A

Gardnerella vaginalis,
H. influenzae,
E. coli.

221
Q

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

A

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

222
Q

CERVICAL CANCER SCREENING
when is screening offered?

A

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

223
Q

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

A
  • “Can’t see, spit, pee or shit” > caution in elderly as falls esp oxybutynin immediate release in frail
224
Q

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

A
  • C/I in uncontrolled HTN as stimulates SNS to increase BP, can lead to hypertensive crisis so monitor BP
225
Q

DYSMENORRHOEA
What is secondary dysmenorrhoea?

A

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

MY REVISION - ALL TO DO (21 decks)

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