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 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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4
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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5
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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6
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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7
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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8
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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9
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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10
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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11
Q

VASA PRAEVIA
What are some risk factors for vasa praevia?

A
  • Placenta praevia
  • Multiple pregnancy
  • IVF pregnancy
  • Bilobed placentas
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12
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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13
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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14
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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15
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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16
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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17
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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18
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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19
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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20
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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21
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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22
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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23
Q

GESTATIONAL DIABETES
What are the maternal risks of GDM?

A
  • Pre-eclampsia
  • DKA or hypos
  • UTIs
  • IHD
  • Nephropathy, retinopathy
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24
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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25
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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26
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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27
Q

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

A
  • Previous PROM/preterm
  • Smoking
  • Polyhydramnios
  • Amniocentesis
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28
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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29
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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30
Q

STAGES OF LABOUR
What are 7 important hormones in labour?

A
  • Prostaglandins
  • Oxytocin
  • Oestrogen
  • Beta-endorphins
  • Adrenaline
  • Prolactin
  • Relaxin
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31
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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32
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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33
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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34
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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35
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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36
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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37
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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38
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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39
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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40
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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41
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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42
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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43
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
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44
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)
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45
Q

HYPEREMESIS
What are some associations of hyperemesis gravidarum?

A
  • nulliparity,
  • hyperthyroid,
  • obesity,
  • decreased in smokers
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46
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)

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47
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

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48
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.

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49
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
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50
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

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51
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

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52
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)

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53
Q

PUERPERAL INFECTION
what is it defined as?

A

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

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54
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…)

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55
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)
56
Q

CHORIONIC VILLUS SAMPLING
when is chorionic villus sampling performed?

A

Usually between 10-13 weeks

57
Q

AMNIOCENTESIS
When is amniocentesis performed?

A

from 15 weeks onwards

58
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
59
Q

GONORRHOEA IN PREGNANCY?
what is the management?

A

500mg ceftriaxone IM single dose

60
Q

SYPHILIS IN PREGNANCY
what is the management?

A

penicillin

61
Q

TRICH VAGINALIS IN PREGNANCY
what is the management?

A

metronidazole

62
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
63
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.

64
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
65
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

66
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
67
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)
68
Q

FIBROIDS
What are some risk factors for fibroids?

A
  • Afro-Caribbean
  • Obesity
  • Early menarche
  • FHx
  • Increasing age (until menopause)
69
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

70
Q

ENDOMETRIOSIS
What are some risk factors for endometriosis?

A
  • Early menarche,
  • late menopause,
  • obstruction to vaginal outflow (imperforate hymen)
71
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
72
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)
73
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)
74
Q

PCOS
What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism
  • Insulin resistance
  • Oligo or amenorrhoea + sub/infertility
75
Q

PCOS
How does insulin resistance present?

A
  • Obesity, acanthosis nigricans (thickened, rough skin often axilla + elbows with velvety texture), psychological Sx
76
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

77
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)
78
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
79
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
80
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
81
Q

OVARIAN CANCER
What are some types of epithelial cell tumours?

A
  • Serous carcinoma (#1)
  • Endometrioid, clear cell, mucinous + undifferentiated tumours too
82
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
83
Q

OVARIAN CANCER
What are metastatic tumours?

A
  • Secondary tumours
  • Krukenberg = metastasis in ovary, usually from GI (stomach) > CLASSIC “SIGNET-RING” CELLS ON HISTOLOGY
84
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)

85
Q

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

A
  • COCP
  • Early menopause
  • Breast feeding
  • Childbearing
86
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
87
Q

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

A
  • Endometriosis
  • Fibroids + adenomyosis
  • Pelvic infection
  • Pregnancy
  • Benign cysts
88
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
89
Q

OVARIAN CYST
What are the three types of functional cysts?

A
  • Follicular (most common)
  • Corpus luteum
  • Theca lutein
90
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
91
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)
92
Q

OVARIAN CYST
What are some features of neoplastic cysts?

A
  • Often complex
  • > 10cm
  • Irregular borders
  • Internal septations appearing multi-locular
  • Heterogenous fluid
93
Q

OVARIAN CYST
What are the 2 benign epithelial neoplasms?

A
  • Serous cystadenoma (most common epithelial tumour)
  • Mucinous cystadenoma
94
Q

OVARIAN CYST
How does serous cystadenoma present?

A
  • May be bilateral, filled with watery fluid, 30–50y
95
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
96
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
97
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)
98
Q

OVARIAN CYST
What are the germ cell tumour markers?

A
  • Lactate dehydrogenase
  • Alpha-fetoprotein
  • Human chorionic gonadotropin
99
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
100
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
101
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)

102
Q

ENDOMETRIAL CANCER
What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking (Seem to have anti-oestrogenic effect)
103
Q

ENDOMETRIAL POLYP
What are some risk factors of endometrial polyps?

A
  • Being peri or post-menopausal
  • HTN
  • Obesity
  • Tamoxifen
104
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
105
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
106
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
107
Q

MENOPAUSE
What is the mechanism of action of clonidine?

A
  • Alpha-adrenergic receptor agonist
108
Q

HRT
What are the side effects associated with oestrogen?

A
  • Nausea,
  • bloating,
  • headaches,
  • breast swelling or tenderness,
  • leg cramps
109
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
110
Q

ATROPHIC VAGINITIS
What are some risk factors for atrophic vaginitis?

A
  • Menopause
  • Oophorectomy
  • Anti-oestrogen (tamoxifen, anastrozole)
111
Q

URINARY INCONTINENCE
What causes urge incontinence/OAB?

A
  • Overactivity + involuntary contractions of the detrusor muscle
112
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)
113
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
114
Q

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

A
  • Parasympathetic so Pissing = decreases need to urinate + spasms
115
Q

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

A
  • Sympathetic so Storage = relaxes detrusor + increases bladder capacity
116
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)
117
Q

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

A
  • Age
  • BMI
  • Multiparity (vaginal)
  • Spina bifida
  • Pelvic surgery
  • Menopause
118
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)
119
Q

DYSMENORRHOEA
What is the management of primary dysmenorrhoea?

A
  • NSAIDs like mefenamic acid during menstruation
  • COCP second line
120
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)
121
Q

ENDOMETRIOSIS
What are some protective factors?

A

Multiparity + COCP

122
Q

HRT
What are the side effects associated with progesterone?

A

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

123
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
124
Q

HYDATIDIFORM MOLE
What is a partial mole?

A
  • Triploid (69XXX, 69XXY) trophoblast cells
  • 2 sperm fertilise 1 egg
  • Some recognisable foetal tissue
125
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
126
Q

HYDATIDIFORM MOLE
What are some risk factors for hydatidiform mole?

A
  • Extremes of reproductive age
  • Previous molar pregnancy
  • Multiple pregnancies
  • Asian women
  • OCP
127
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
128
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
129
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
130
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)
131
Q

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

A

Gardnerella vaginalis,
H. influenzae,
E. coli.

132
Q

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

A

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

133
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

134
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
135
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
136
Q

DYSMENORRHOEA
What is secondary dysmenorrhoea?

A

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

137
Q

CERVICAL CANCER
what are the risk factors for cervical cancer?

A
  • HPV
  • multiple sexual partners
  • younger age at first intercourse
  • non-attendance at smears
  • immunosuppression
  • oral contraceptives
  • higher parity
  • tobacco use
  • deprivation