Women's Health Flashcards

(324 cards)

1
Q

Ligaments of the uterus

A

o Broad ligament – double layer of peritoneum attaching sides of uterus to pelvis
o Round ligament – from uterine horns to labia majora via inguinal canal, maintains anteverted position of uterus
o Ovarian ligament – joins ovaries to uterus
o Cardinal ligament – from cervix to lateral pelvic walls, contains uterine artery and vein
o Uterosacral ligament – cervix to sacrum, supports uterus

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2
Q

phases of the menstrual cycle

A

follicular phase days 1-13/14, ovulation day 13/14, luteal phase days 14-28

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3
Q

follicular phase of egg before entering menstrual cycle

A
  • primordial follicle - 1 oocyte surrounded by granulosa cells (secrete oestrogen, progesterone and inhibin)
  • primary follicle - zona pellucida forms
  • preantral follicle - granulosa cells differentiate into Theca cells (oestrogen)
  • early antral follicle - oocyte full size, antrum forms and fills with fluid (from birth to when it enters cycle)
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4
Q

follicular phase during menstrual cycle

A
  • makes mature/Graafian follicle
  • after day 7 10-15 early antral follicles grow
  • 1 is dominant and antrum grows
  • LH surge - oocyte emerges out of meiotic arrest - first division into secondary oocyte
  • ovulation
  • enzymes rupture follicle and oocyte carried away in antral fluid
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5
Q

luteal phase

A
  • after ovulation granulosa cells increase in size becoming corpus luteum (oestrogen, prog, inhibin)
  • no fertilisation after 10d corpus luteum undergoes apoptosis = triggers menstruation
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6
Q

uterine changes during menstrual cycle

A
  • Days 1-5 – menstrual phase, decreased progesterone - endometrial degeneration and menstrual flow
  • Days 5-14 – proliferative phase, oestrogen makes endometrium thicken and stimulates myometrium and progesterone receptor generation
  • Days 15-28 – secretory phase, progesterone binds overriding oestrogen to prevent myometrium contraction and the endometrium secrets glycogen to nourish oocyte
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7
Q

oestrogen and the menstrual cycle

A

produced by granulosa cells in follicular phase and by corpus luteum in luteal phase

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8
Q

progesterone and the menstrual cycle

A

produced by granulosa and theca cells in small amounts in follicular phase, by corpus luteum in large amounts in luteal phase

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9
Q

FSH in menstrual cycle

A

o High early in follicular phase due to decrease in oestrogen and progesterone causing an increase in GnRH from hypothalamus
o Slow decrease during cycle due to dominant oocyte releasing more oestrogen
o Increase in FSH at day 10-11 causing LH receptors to develop on Theca cells

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10
Q

LH and the menstrual cycle

A

o Levels constant for most of follicular phase
o LH surge 18h before ovulation due to high oestrogen increasing sensitivity to GnRH – surge allows oocyte to complete meiosis 1
o LH decreases rapidly then slowly after ovulation due to increase in progesterone
o LH acts on Theca cells to produce androgens – converted to oestrogen and atrial fluid in granulosa cells

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11
Q

inhibin and the menstrual cycle

A

decreases FSH by inhibiting release at pituitary, peaks for ovulation, decreases as corpus luteum degenerates

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12
Q

meiotic divisions for oogenesis

A

females arrested in prophase of meiosis I – maturation during menstrual cycle – arrested in metaphase of meiosis II until ovulation, meiosis complete after fertilisation

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13
Q

route of sperm

A

seminiferous tubules – rete testis – efferent ducts – epididymis – vas deferens – ejaculatory duct – urethra

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14
Q

LH and FSH in males

A

o FSH – stimulates Sertoli cells to produce inhibin (inhibits release of FSH from pit) and promotes spermatogenesis
o LH – stimulates testosterone release from Leydig cells (negative feedback to hypothalamus and pit

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15
Q

fertilisation

A
  • day 1 - fusion, enzymes digest zona pellucida, sperm enters, mem pot change prevents more entering, 4-7h after meiosis II occurs and the DNA replication and mitosis
  • 2/3 - zygote, in fallopian tube, CLEAVAGE increases no. of totipotent cells
  • 4 - compaction
  • 5 - cavitation and expansion - fluid filled cavity expands, blastocyst >80cells
  • 6+ - hatch out of zona pellucida
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16
Q

implantation timing/changes

A
  • 21st day of menstrual cycle, 7 days post fertilisation
  • endometrial cells provide metabolic fuel for early grown for first 5 weeks until foetal heart is functioning
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17
Q

stages of implantation

A
  1. Apposition – day 9, hatched blastocyst orientates via embryonic pole, synchronises with endometrium
  2. Attachment – integrins between endometrial endothelium and trophoblast cells
  3. Differentiation – trophoblast layer splits into cytotrophoblast and synctiotrophoblast
  4. Invasion – synctiotrophoblast erodes spiral blood vessels by digestion of basal lamina via enzymes to increase blood flow
  5. Decidual reaction – differentiation of stromal cells adjacent to blastocyst
  6. Maternal recognition – secretion of IL-2 prevents rejection, day 11 post fertilisation
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18
Q

beta hCG (human chorionic gonadotrophin)

A
  • Produced by synctiotrophoblast cells and begins being released at endometrial invasion
  • Maintains corpus luteum and stimulates oestrogen and progesterone production; prevents menstruation
  • Levels peak 60-80 days after last menstruation then rapidly decreases
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19
Q

relaxin in pregnancy

A

– Increases early in pregnancy from ovaries and placenta, limits uterine activity, softens and ripens cervix

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20
Q

oxytocin in pregnancy

A

from posterior pituitary, secreted throughout, increases towards end to stimulate uterine contractions and caring behaviours

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21
Q

prostaglandins in pregnancy

A

– PGF2a most abundant, PGE2 10x stronger, initiate labour, produced by uterine tissue

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22
Q

maternal adaptations during pregnancy

A
  • weight gain 10-15kg
  • uterus hypertrophy and hyperplasia, cervix softens
  • blood vol 50% increase, RBC mass increase, hb concentration decrease, WBC increase
  • CV - CO 40% inc, peripheral resistance 50%decrease
  • lungs - tidal vol 40%inc, no rate change
  • renal - GFR 40% inc
  • GI - reduced motility, delayed gastric emptying, constipation
  • thyroid enlargement
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23
Q

diagnosis of labour

A

contractions with effacement and dilatation of the cervix

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24
Q

signs of labour

A
  • Show (mucus plug from the cervix)
  • Rupture of membranes
  • Regular, painful contractions
  • Dilating cervix on examination
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25
first stage of labour
- latent phase - 0-4cm, 0.5cm/h, irreg contractions - active phase - 4-7cm, 1cm/h, reg contractions - transition phase - 7-10cm, 1cm/h, strong contractions - head descends remaining flexed, rotation from OT to OA - membranes rupture
26
second stage of labour
* Contraction continue, head descends and flexes further, rotation normally complete * Passive = before pushing starts * Active = Pushing starts when head reaches pelvic floor * Delivery – head extends as its delivered over perineum, rotates back to transverse before the shoulders deliver
27
third stage of labour
- placenta, normally 15min with up yo 500ml blood loss - uterine muscle fibres contract shearing blood vessels to placenta
28
the passenger descriptions
* Presentation – head (cephalic), buttocks (breech) * Position of the head – rotation – OT, OP, OA * Attitude of the head – degree of flexion – vertex (optimal), brow or face * Foetal lie – longitudinal (optimal), transverse (sideways), oblique (slight angle)
29
gestation
w+d since LMP (start of period)
30
gravidity and parity
gravidity is how many times they have been pregnant including this one, parity is how many deliveries past 24w despite the outcome (still birth included)
31
trimesters of pregnancy
1st 0-12w 2nd 13-26w 3rd 27-birth
32
investigations during routine antenatal appt
* Symphysis–fundal height measurement from 24 weeks onwards * Fetal presentation assessment from 36 weeks onwards * Urine dipstick for protein for pre-eclampsia * Blood pressure for pre-eclampsia * Urine for microscopy and culture for asymptomatic bacteriuria
33
vaccines during pregnancy
* Whooping cough (pertussis) from 16 weeks gestation * Influenza (flu) when available
34
pregnancy lifestyle advice
* Take folic acid 400mcg from before pregnancy to 12 weeks (reduces neural tube defects) * Take vitamin D supplement (10 mcg or 25 for those at risk daily) * Aspirin 75mg for women at risk of pre-eclampsia * LMWH for risk of VTE etc.....
35
booking clinic
* Blood group, antibodies, and rhesus D status * FBC for anaemia * Screening for thalassaemia (all women) and sickle cell disease (women at higher risk) * Also offered screening for HIV, Hep B, Syphilis antibodies - Measurements – weight, height, BMI, urine for protein and bacteria, BP
36
combined screening test during pregnancy
- 10-14w (Down's T21, Edwards' T18, Patau's T13) - USS for nuchal thickness (>6mm in downs) - bloods - HCG (high = risk), PAPPA (low = risk)
37
Quadruple blood screening test during pregnancy
- done for downs if >14w - beta-HCG (high is greater risk), Alpha-fetoprotein (AFP, low is risk), serum oestriol (low is risk), inhibin-A (high is greater risk)
38
further testing for screening during pregnancy
- for higher chance result (risk >1/150) - second screening test - non-invasive prenatal testing (NIPT) - diagnostic test with amniocentesis (later on) or chorionic villus sampling (<15w) for DNA karyotyping
39
presentation o an ectopic pregnancy
* Pregnancy symptoms, constant right or left iliac fossa pain, bleeding, cervical motion tenderness during examination, dizziness (blood loss), shoulder tip pain (peritonitis) * Gestational sac found on USS outside of uterus
40
pregnancy of unknown location and hCG changes
* Positive pregnancy test, no pregnancy found of USS * Beta hCG used for monitoring and repeated after 48h (normally hCG would double) o Rise >63% likely indicates intrauterine pregnancy – should be visible on USS when hCG > 1500 IU/L o Rise <63% indicates ectopic o Fall >50% indicated miscarriage
41
management of ectopic pregnancy
- expectant management - medical - IM methotrexate (highly teratogenic) - surgical - salpingectomy, salpingotomy (preserve tube)
42
management of miscarriage <6w
– expectant management if no complications then repeat urine pregnancy test after 7-10 days
43
management of miscarriage >6w
- expectant - medical - oral or vaginal misoprostol (prostaglandin analogue making cervix soften and uterus contract) - surgical - manual vacuum aspiration <10w, D&C with electric vacuum
44
recurrent miscarriage
>3 - Causes: idiopathic, older age, antiphospholipid syndrome (give low dose aspirin), thrombophilia’s, uterine abnormalities, genetic factors, chronic histiocytic intervillositis, chronic diseases (diabetes, thyroid disease, SLE)
45
medical abortion
* Mifepristone (anti-progestogen – stops pregnancy and relaxes cervix) * Misoprostol (prostaglandin analogue – softens cervix and stimulates uterine contractions) 1 – 2 day later * Rhesus negative women above 10w should have anti-D prophylaxis
46
surgical abortion
* Meds used before for cervical priming - misoprostol, mifepristone, or osmotic dilators o Cervical dilatation and suction of the contents of the uterus (up to 14w) o Cervical dilatation and evacuation using forceps (between 14 - 24 weeks)
47
post-abortion care
may experience vaginal bleeding and cramps for up to 2w, urine pregnancy test after 3w, support and counselling offered
48
nausea and vomiting of pregnancy
- start from 4 – 7 weeks, are worst around 10 – 12 weeks and resolve by 16 – 20 weeks - hCG thought to be cause - more severe in molar and multiple pregnancies due to higher levels
49
hyperemesis gravidarum
* More than 5 % weight loss compared with before pregnancy * Dehydration * Electrolyte imbalance - assess severity using Pregnancy-Unique Quantification of Emesis (PUQE) score
50
treatment of hyperemesis gravidarum
- antiemetics (prochlorperazine 1sr) - ranitidine/omeprazole for reflux - admission for IV fluid, antiemetics and thiamine supplements with daily U&Es
51
what are partial and complete molar pregnancies
- complete mole - 2 sperm in an empty ovum (no genes) - partial mole - 2 sperm in a normal ovum - some fetal material may form
52
diagnosis of molar pregnancy
- more severe morning sickness, bleeding, abnormally high hcg - snowstorm appearance on USS
53
treatment of molar pregnancy
- remove mole - histology - referral to gestational trophoblastic disease centre - can occasionally metastasise needing chemo
54
types of multiple pregnancy
* Monozygotic: identical twins (from a single zygote) * Dizygotic: non-identical (from two different zygotes) * Monoamniotic: single amniotic sac * Diamniotic: two separate amniotic sacs * Monochorionic: share a single placenta * Dichorionic: two separate placentas - diamniotic dichorionic best outcome
55
multiple pregnancy on USS
* Dichorionic diamniotic twins - membrane between the twins, with a lambda sign * Monochorionic diamniotic twins - membrane between the twins, with a T sign * Monochorionic monoamniotic twins - no membrane separating
56
specific complications in twins
- twin-twin transfusion syndrome (one twin receives majority of blood from placenta) - twin anaemia polycythaemia sequence (less acute- one becomes anaemic, other polycythaemia)
57
antenatal care for multiples
* FBC at booking clinic, 20w, 28w (increased risk of anaemia) * Additional USS – 2 weekly from 16w with monochorionic, 4 weekly from 20w for dichorionic * Planned CS before spontaneous labour occurs, corticosteroids given before * Monoamniotic twins require CS between 32-33+6 weeks
58
definition of polyhydramnios
liquor volume increased, deepest liquor pool >10cm generally considered abnormal, should be around 1000ml at 38w
59
causes of polyhydramnios
* Maternal disorders: GDM, renal failure * Twins: twin-twin transfusion syndrome * Fetal anomaly: upper GI obstructions/inability to swallow, CNS/cardiac/renal abnormalities, myotonic dystrophy
60
management of polyhydramnios
- detailes USS - blood glucose monitoring - <34 w sever amnioreduction or NSAIDS (reduce fetal urine output) - vaginal delivery unless complications
61
oligohydramnios
- develops when increased fluid loss or decreased production
62
investigations for oligohydramnios
Fluid analysis from speculum examination – ferning test (dried amniotic fluid forms fern-like crystals) - vaginal swab for placental alpha macroglobulin-1 (PAMG-1) and insulin-like growth factor binding protein-1 (IGFBP-1))
63
management of oligohydramnios
* Monitoring * Amnioinfusion (saline or Ringer’s lactate infused) * Induction of labour between 36-38w (risk of cord compression and limb deformities)
64
UTI in pregnancy and most likely bacteria
-Higher risk of pyelonephritis and miscarriage/ preterm birth - most E.coli (gram-negative, anaerobic, rod), klebsiella pneumoniae (gram negative, anaerobic rod)
65
management of UTI in pregnancy
- culture for sensitivities - 7d abx - nitro (not in 3rd trimester), amox, cefalexin, trimethoprim (not in 1st)
66
group B streptococcus infection in pregnancy
- normal in flora of 20-40% - can cause neonatal sepsis/pneumonia/encephalitis or UTI in mother - screened at 35-37w if risk factors
67
treatment of GBS in pregnancy
3g IV Benzylpenicillin stat after onset of labour, followed by 1.5g IV Benzylpenicillin 4hourly until delivery (takes 4h to cross over into fetus)
68
chlamydia and gonorrhoea in pregnancy
- preterm labour and neonatal conjunctivitis * Chlamydia treated with azithromycin or erythromycin (tetracyclines cause fetal tooth discolouration) * Gonorrhoea treated with cephalosporins
69
management of VTE in pregnancy
- Prophylactic LMWH (dalteparin) from 28w if 3 risk factors, 1st trimester if >4 - compression stockings - CTPA and doppler used for diagnosis - dalteparin immediately
70
what is pre-eclampsia
- new htn with end-organ dysfunction (proteinuria) - occurs after 20w when spiral arteries of placenta form abnormally leading to a high vascular resistance in them
71
pre-eclampsia triad
htn, proteinuria, oedema
72
pregnancy-induced htn
htn occurring after 20w without end-organ damage (proteinuria)
73
symptoms of pre-eclampsia
* Headache * Visual disturbance or blurriness * Nausea and vomiting * Upper abdominal or epigastric pain (this is due to liver swelling) * Oedema * Reduced urine output * Brisk reflexes
74
prophylaxis of pre-eclampsia
- high risk (other chronic diseases) aspirin from 12w - moderate risk (>1 risk factor) aspirin from 12w
75
diagnosis of pre-eclampsia
BP >140/90 proteinuria, organ dysfunction, placental dysfunction low placental growth factor
76
management of pre-eclampsia
- urine dip, FBC,LFT, U&E weekly with serial growth scans - BP every 48h - scoring systems for admission (fullPIERS or PREP-S) - labetalol (1st line antihypertensive) then nifedipine - IV mag sulf during labour and in 24h after to prevent seizures - CS if uncontrolled - after delivery give enalapril
77
eclampsia
- seizures associated with pre-eclampsia from cerebral vasospasm - IV magnesium sulphate
78
HELLP syndrome in pregnancy
- complication of pre/eclampsia - Haemolysis - EL elevated liver enzymes - LP low platelets
79
complications of gestational diabetes
- large fetus, macrosomia - shoulder dystocia during delivery
80
oral glucose tolerance test for GD
- at 24-28w if at risk - Normal results: o Fasting: < 5.6 mmol/l o At 2 hours: < 7.8 mmol/l o Anything higher is GM: cut off for gestational diabetes as simply 5 – 6 – 7 – 8
81
management of GD
- education on lifestyle nd monitoring BM - 4 weekly USS from 28-36w - fasting glucose>7 = insulin +/- metformin - FG >6 plus macrosomia = insulin +/- metformin - glibenclamide (sulfonylurea) if refuse insulin
82
pre-existing diabetes in pregnancy
- good control before - retinopathy screening after booking then at 28w - planned delivery at 37-38+6w - sliding scale insulin regime during labour
83
postnatal care with GD
- resolves immediately after birth - stop meds - babies at risk of neonatal hypoglycaemia, polycythaemia, jaundice and congenital heart disease
84
obstetric cholestasis
- reduced outflow of bile acids from liver dur to increased oestrogen and progesterone - resolves after delivery - increases risk of still birth - presents with jaundice
85
investigations for obstetric cholestasis
LFT (abnormal ALT, AST, GGT) and bile acids checked (raised) normal for ALP to increase because also made by placenta
86
management of obstetric cholestasis
- emollients for itching - Ursodeoxycholic acid improves LFTs planned delivery at 37w if severe
87
antepartum haemorrhage and most common causes
- PV bleeding from 24w - most common causes - placenta previa, placental abruption, vasa previa
88
comparison of placenta previa, placental abruption and vasa previa
89
investigations for APH
- CTG immediately, USS - if severe then catheterise and monitor hourly urine output - FBC, group and crossmatch, coag screen, U&E
90
management of APH
- treat cause - IV access, analgesia, resuscitation - if in shock then enact massive haemorrhage protocol - may need urgent CS
91
definition of low-lying placenta and placenta praevia
- low lying is within 20mm of internal cervical os - placenta praevia - placenta is over the internal os
92
diagnosis of placenta praevia
- normally on 20w anomaly scan - bleeding normally starts around 36w
93
management of placenta praevia
- transvaginal USS at 32 and 36w - corticosteroids between 24-35+6w - planned CS at 36-37w - emergency CS if haemorrhage or premature labour
94
what is placental abruption
placenta/part of it separates from uterus wall - area can bleed extensively
95
presentation of placental abruption
* Sudden onset severe abdominal pain that is continuous * APT * Shock (hypotension and tachycardia) * Abnormalities on the CTG indicating fetal distress * Characteristic “woody” abdomen on palpation, suggesting a large haemorrhage
96
what is a concealed abruption
- cervical os remains closed - severity can be underestimated
97
initial management of major/massive APH
o Urgent involvement of a senior obstetrician, midwife and anaesthetist o 2 x grey cannula o Bloods include FBC, UE, LFT and coagulation studies o Crossmatch 4 units of blood o Fluid and blood resuscitation as required o CTG monitoring of the fetus o Close monitoring of the mother
98
management of placental abruption
- management of bleed - USS to diagnose - corticosteroids between 24-34+6w - may need anti-D - emergency CS
99
what is vasa praevia
foetal vessels within the membranes and travel across the internal cervical os - exposed due to lack of Wharton's jelly lead to bleeding which can be fatal for fetus due to small blood volume
100
presentation of vasa praevia
* Ideally diagnosed by USS but not reliable * May present with antepartum haemorrhage or during labour when membranes seen or if fetal distress + dark red bleeding (high fetal mortality)
101
management of vasa praevia
* Corticosteroids from 32 weeks then elective CS planned for 34-36 w * Emergency CS
102
what is placenta accreta
Placenta implants deeper, through and past the endometrium, making it difficult to separate the placenta after delivery – PPH. - accreta (surface of myometrium) - increta (deeply into myometrium) - percreta (past myometrium and perimetrium)
103
management of placenta accreta
- diagnosis at USS - planned CS at 35-36+6 - hysterectomy/uterus preserving surgery/expectant management (leaving to be reabsorbed but risk of infection and bleeding)
104
indications for continuous CTG monitoring
sepsis, maternal tachycardia, significant meconium, pre-eclampsia, APH, delay in labour, use of oxytocin
105
key features on a CTG
* Contractions – per 10 minutes * Baseline rate – the baseline fetal heart rate, reassuring 110-160, non-reassuring or abnormal <100 or >180 * Variability – how the fetal heart rate varies up and down, reassuring 5-25, non-reassuring, abnormal <5 for over 50mins or >25 for over 25mins * Accelerations – fetal heart rate spikes, generally a good sign * Decelerations - more concerning (response to hypoxia)
106
categories for CTG
* Normal * Suspicious: a single non-reassuring feature * Pathological: two non-reassuring features or a single abnormal feature * Need for urgent intervention: acute bradycardia or prolonged deceleration of more than 3 minutes
107
timescale for managing fetal bradycardia
* 3 minutes – call for help * 6 minutes – move to theatre * 9 minutes – prepare for delivery * 12 minutes – deliver the baby (by 15 minutes)
108
fetal scalp blood sample - when and what does it measure
- do if pathological fetal HR unless acute (immediate delivery) - Mostly to measure pH and lactate (fetal compromise and hypoxia) or anaemia from placental damage
109
fetal blood pH from scalp blood sample
>7.25 – normal, can repeat in 1h 7.21-7.24 – borderline, repeat in 30min <7.20 – abnormal, consider delivery
110
when to induce labour
41-42w, prelabour ROM, fetal growth restriction, pre-eclampsia, obstetric cholestasis, diabetes, intrauterine fetal death
111
score used to determine where to induce labour
- Bishop score (total score of 13, score of >8 predicts successful induction) o Fetal station (scored 0 – 3) o Cervical position (scored 0 – 2) o Cervical dilatation (scored 0 – 3) o Cervical effacement (scored 0 – 3) o Cervical consistency (scored 0 – 2)
112
methods of labour induction
- membrane sweep done at term - vaginal prostaglandin via gel, tablet or pessary - cervical ripening balloon - ARM +/- oxytocin infusion - oral mifepristone (anti-progesterone) + misoprostol for still birth
113
uterine hyperstimulation from induction of labour
- main complication of induction - contractions lasting >2m or >5 in 10min - can lead to fetal distress, emergency CS and uterine rupture - stop inductions and give terbutaline for tocolysis
114
partogram
* Used for monitoring first stage of labour * 2 lines on partogram that indicate when labour isn’t progressing: o Alert line – indication for an amniotomy (artificially rupturing the membranes) and repeat examination in 2h o Action line – needs to be escalated to obstetric-led care
115
4 P's that influence progress in labour
* Power (uterine contractions) * Passenger (size, presentation and position of the baby) * Passage (the shape and size of the pelvis and soft tissues) * Psyche (the support and antenatal preparation)
116
failure to progress in first stage of labour
<2cm in 4h slowing of progress partogram alert line (ARM), action line (further care) if 2h after ARM no dilation then start oxytocin drip
117
failure to progress in second stage of labour
when pushing lasts >2h nulliparous/1h multiparous - power - oxytocin for weak contractions - passenger/passage - may be impossible needing CS - change positions, encouragement, analgesia, oxytocin, episiotomy, instrumental delivery, CS
118
failure to progress in third stage of labour
>30mins with active management, >60mins with physiological management
119
active management of third stage of labour
IM oxytocin and controlled cord traction
120
obstructed labour
- labour dystocia - labour >24h, insurmountable barrier - can be fatal to both - complications - uterine rupture, infection, compression injuries - IV access, fluids, catheter, assisted delivery/CS
121
shoulder dystocia
- anterior shoulder stuck behind pubis symphysis after head delivered EMERGENCY
122
presentation of shoulder dystocia
- difficulty delivering face - failure of restitution (doesn't rotate to OT) - turtle neck sign - head retracts back into vagina
123
management of shoulder dystocia
- needs obstetrician, anaesthetist, paediatrician - episiotomy - McRoberts manoeuvre (knees to abdomen to provide posterior pelvic tilt) - pressure on anterior shoulder - Rubins manoeuvre - hand in vagina pressing baby shoulder - Wood's screw manoeuvre - Zavanelli manoeuvre - push head back in for emergency CS
124
complications of shoulder dystocia
* Fetal hypoxia (can cause cerebral palsy) * Brachial plexus injury and Erb’s palsy * Perineal tears * Postpartum haemorrhage
125
breech presentation
- Complete/flexed breech (15%) - Frank/extended breech (70%)– with hips flexed and knees extended, bottom first - Footling breech (15%) – with a foot hanging through the cervix - External cephalic version (ECV) from 37w, 50% success
126
cord prolapse
- cord descends below the presenting part into the vagina after ROM - high risk of compression causing fetal hypoxia
127
management of a cord prolapse
- emergency CS - cord kept warm and wet but don't touch (causes vasospasm) - if baby already compressing then push back in, woman in left lateral lie and tocolytic meds to minimise contractions
128
instrumental delivery
10% of births in UK single dose co-amox after to prevent maternal infection indicated when failure to progress, fetal distress, exhaustion
129
risks to mother from instrumental delivery
PPH, episiotomy, perineal tears, anal sphincter injury, incontinence, nerve injury – obturator (weakness in hip adduction and rotation and numbness of medial thigh) or femoral nerve (weakness of knee extension, loss of patellar reflex and numbness of anterior thigh)
130
risks to baby during instrumental delivery
- cephalohematoma (blood between skull and periosteum) with ventouse, facial nerve palsy with forceps - Serious risks to baby: subgaleal haemorrhage, intercranial haemorrhage, skull fracture, spinal cord injury
131
causes of intrapartum haemorrhage
uterine rupture, placental abruption
132
uterine rupture
- incomplete (perimetrium remains intact) or complete (uterus contents into peritoneal cavity) - significant bleeding an high mortality for both - higher risk if VBAC
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presentation of uterine rupture
Acutely unwell mother and abnormal CTG – abdo pain, bleeding, ceasing of uterine contractions, hypotension, tachycardia, collapse
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management of uterine rupture
- emergency CS then repair or hysterectomy - resuscitation and transfusions if needed
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classification of perineal tears
* First-degree – injury limited to the frenulum of the labia minora and superficial skin * Second-degree – including the perineal muscles, but not affecting the anal sphincter * Third-degree – including the anal sphincter, but not affecting the rectal mucosa * Fourth-degree – including the rectal mucosa
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management of perineal tears
- sutures above 1st degree - broad-spec abx - laxatives - physio - follow up monitoring - >3rd degree offer subsequent CS
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long term complications of perineal tears
- urinary and bowel incontinence - fistula between vagina and bowel - sexual dysfunction and dyspareunia - mental health
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classification of PPH
- 500ml after vaginal delivery, 1000ML after CS * Minor PPH <1000ml * Major PPH >1000ml o Moderate PPH – 1000 – 2000ml o Severe PPH – over 2000ml * Primary (within 24h of delivery) or secondary (24h-12 weeks)
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causes of PPH (4 Ts)
* T – Tone (uterine atony – the most common cause) * T – Trauma (e.g. perineal tear) * T – Tissue (retained placenta) * T – Thrombin (bleeding disorder)
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preventative measures for PPH
- treat anaemias in pregnancy - empty bladder during birth - Active management of the third stage (10 units of IM oxytocin- increases uterus contraction)and controlled cord traction - IV tranexamic acid during CS if high risk
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management of PPH
1. Resuscitation ABCDE 2. Lie the woman flat, keep her warm and communicate 3. 2 large-bore cannulas 4. Bloods for FBC, U&E and clotting screen 5. Group and cross match 4 units 6. Warmed IV fluid and blood resuscitation as required 7. Oxygen (regardless of saturations) 8. Fresh frozen plasma is used where there are clotting abnormalities or after 4 units of blood transfusion
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mechanical treatment to stop bleeding in PPH
- fundal massage - catheterisation
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medical treatment to stop bleeding in PPH
- oxytocin 40 units in 500ml and ergometrine - carboprost IM - prostaglandin analogue - misoprostol sublingual (prostaglandin analogue) - tranexamic acid (antifibrinolytic)
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surgical treatment to stop bleeding in PPH
- intrauterine balloon tamponade for 24h - B-lynch or Hayman suture around uterus to compress - uterine artery ligation - hysterectomy last resort
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secondary PPH
*Likely due to retained products of conception or infection (eg endometritis) *Investigations – US, endocervical and high vaginal swabs *Management – depends on cause (surgical evacuation, antibiotics)
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postpartum endometritis
- inflammation of endometrium, mostly from infection - more common after CS - GAS (most common cause of puerperal sepsis), e.coli, staph
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presentation of postpartum endometritis
foul-smelling discharge or lochia, abnormal bleeding, pain, fever, sepsis
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management of postpartum endometritis
- vaginal swabs - urine culture - USS if retained products of conception suspected - if septic needs admission - co-amox
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mastitis
- inflammation of breast tissue - can be caused by milk blockage or infection - manage obstruction with continued BF, massage and heat packs - for infection milk sample for culture, flucloxacillin
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baby blues
- most women in first week, last about 2w - mood swings, low mood, tearfulness - caused by hormonal changes, recovery, stress
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postnatal depression
- low mood, anhedonia and low energy - peak around 3m after birth - mild - additional support - moderate - antidepressants and CBT - severe - may need input from specialist psych servoces
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scale used to assess severity of postnatal depression
Edinburgh postnatal depression scale assesses how mother has felt over the past week, 10 questions with total score out of 30 points, score of 10 or more suggests PD
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puerperal psychosis
- starts few weeks after birth - Delusions, hallucinations, depression, mania, confusion, thought disorder - emergency, may need admission to mother and baby unit
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perinatal mental health services
- mental health conditions before pregnancy - plan and prepare - SSRI safe in pregnancy but beware of neonatal abstinence syndrome (poor feeding and irritability)
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premature labour
birth before 37 weeks gestation, considered non-viable below 23 w
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classification of premature labour
* Under 28 weeks: extreme preterm * 28 – 32 weeks: very preterm * 32 – 37 weeks: moderate to late preterm
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prophylaxis of preterm labour
*Vaginal progesterone – prevents cervix remodelling and myometrium contraction o offered when cervical length <25mm on USS between 16-24 weeks *cervical cerclage – stitch into cervix to keep it closed (removed at term) o offered when cervical length <25mm on USS between 16-24 w with history - rescue cerclage if cervix dilated but no ROM
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preterm prelabour ROM
- diagnosed by pooling amniotic fluid in vagina (ferning test or test of IGFBP-1 or PAMG-1) - management with erythromycin 250mg QDS for 10 days or until labour, induction of labour from 34w
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preterm labour with intact membranes
- contractions and cervical dilatation without ROM
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management of preterm labour without ROM
- fetal monitoring - tocolysis with nifedipine (short term use for transfer to special unit) - maternal corticosteroids (fetal lungs) - IV magsulf (helps protect baby's brain) - delayed cord clamping or cord milking can increase blood vol for baby at birth
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antenatal steroids
- corticosteroids help to develop the fetal lungs and reduce respiratory distress syndrome after delivery. - used in women with suspected preterm labour less than 36 w - two doses of intramuscular betamethasone, 24 hours apart.
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magnesium sulphate for premature delivery
- reduces risk and severity of cerebral palsy - given within 24 hours of delivery of preterm babies of less than 34 weeks gestation - close monitoring for magnesium toxicity every 4h (obs and tendon reflexes)
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small for gestational age
measures below 10th centile for their gestation
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what is measured on fetal USS
estimates fetal weight (EFW), fetal abdominal circumference (AC)
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categories of SGA
- constitutionally small (small family and growing normally) - fetal growth restriction (not growing as expected due to pathology)
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causes of FGR (fetal growth restriction)
* Placenta mediated growth restriction – conditions that affect the transfer of nutrients across placenta – idiopathic, pre-eclapsia, maternal smoking, alcohol, anaemia, malnutrition, infection, maternal health conditions * Non-placenta mediated growth restriction, where the baby is small due to a genetic or structural abnormality
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long term complications of SGA
increased risk of – CVD, T2DM, obesity, mood and behavioural problems
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investigations when SGA identified
* Blood pressure and urine dipstick for pre-eclampsia * Uterine artery doppler scanning * Detailed fetal anatomy scan by fetal medicine * Karyotyping for chromosomal abnormalities * Testing for infections
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management of SGA
* Aspirin is given to those at risk of pre-eclampsia * Treating modifiable risk factors (e.g. stop smoking) * Serial growth scans to monitor growth * Early delivery where growth is static
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what is rhesus incompatibility
- Rhesus-D negative mother has a rhesus positive baby – blood likely to mix at some point in pregnancy – mother has immune reaction against antigen on baby’s blood so becomes sensitised - normally only problem in subsequent pregnancies as antibodies can cross into fetal blood stream causing haemolytic disease of the newborn
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management of rhesus incompatibility
- prevent sensitisation (IM anti-D for rhesus negative women) at 28w and birth - also given if any trauma/haemorrhage
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kleinhauer test
- assess how much fetal blood in mothers during sensitisation event to quantify amount of anti-D - add acid to mothers blood sample - fetal blood more acid resistant so will survive
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menopause
- retrospective diagnosis (made 12m after LMP) - av age 51 - when periods stop due to lack of ovarian follicular function (no granulosa cells to produce oestrogen/progesterone)
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Postmenopause
from 12m after LMP
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perimenopause and the symptoms
->45y, the time around menopause with vasomotor symptoms and irregular periods - hot flushes, emotional lability, joint pains, brain fog, vaginal dryness etc etc
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premature menopause
- before 40 - result of premature ovarian insufficiency - FSH levels done to aid diagnosis
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contraception needed during menopause
* 2 years after LMP in women <50 * 1 year in women >50 * Progesterone based contraceptives (pill or Mirena) or non-hormonal
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HRT
- Perimenopausal: cyclical combined HRT - Postmenopausal: continuous combined HRT - Takes 3-6 months to have full effect - risks of breast C, endometrial C, VTE, CVD, stoke - risk of VTE reduced by using patches>pills - need progesterone and oestrogen if they have uterus (stop endometrial proliferation) - improves QOL, reduces risk of osteoporosis
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premature ovarian insufficiency
- menopause before 40 - hypergonadotropic hypogonadism (high FSH/LH, low oestrogen) - idiopathic, iatrogenic (post chemo etc), autoimmune, genetic or post infection (TB etc)
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diagnosis and management of premature ovarian insufficiency
- typical menopause symptoms + elevated FSH (2 samples 4w apart) - need HRT until at least average age of menopause
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atrophic vaginitis
- Dryness and atrophy of the vaginal mucosa related to a lack of oestrogen (menopause) - itching, dryness, dyspareunia, bleeding, inflammation, prolapse, recurrent UTI, thin skin - treat with moisturisers + topical oestrogens
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cervical cancer
- mostly younger reproductive age women - 80% squamous cell carcinoma, next most common adenocarcinoma - strongly associated with HPV
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human papilloma virus
- STI, type 16 and 18 cause 70% of cervical cancers - vaccine given in 13y/o - produces proteins that inhibit some tumour suppressor genes
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presentation of cervical cancer
* Symptoms – abnormal vaginal bleeding, discharge, pelvic pain, dyspareunia * Appearance of cervix (needs urgent cancer referral for colposcopy)– ulceration, inflammation, bleeding, visible tumour
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cervical intraepithelial neoplasia
- grading system for level of dysplasia diagnosed at colposcopy - CIN I: mild dysplasia, affecting 1/3 the thickness of the epithelial layer, likely to return to normal without treatment - CIN II: moderate dysplasia, affecting 2/3 the thickness of the epithelial layer, likely to progress to cancer if untreated - CIN III: severe dysplasia, very likely to progress to cancer if untreated – cervical carcinoma in situ
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screening for cervical cancer
- Cervical smear test – tested for high-risk HPV, if positive then microscopy for precancerous changes (dyskaryosis) - Every three years aged 25 – 49 - Every five years aged 50 – 64 - annually if immunocompromised or previous positive HPV
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colposcopy
- used with stains - acetic acid (abnormal cells white), or Schiller's iodine test (abnormal cells don't stain) - punch biopsy or large loop excision
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international federation of gynaecology and obstetrics (FIGO) staging system for gynae cancers
- stage 1 - confined to organ - stage 2 - invades part of adjacent organ - stage 3 - invades further into pelvic wall - stage 4 - invades other pelvic organs (bladder, rectum etc)
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management of cervical cancer
- hysterectomy and local lymph node removal with chemo and radiotherapy - 15% survival for stage 4 - bevacizumab monoclonal antibody to reduce development of new blood vessels
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endometrial cancer
- 80% adenocarcinoma - oestrogen dependant
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endometrial hyperplasia
-precancerous thickening (5% become cancerous) -treated with progestogens - risk when increased oestrogen without progesterone - can be caused by obesity (adipose cells make oestrogen) or PCOS
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presentation of endometrial hyperplasia/cancer
PMB (2ww), abnormal bleeding or discharge, anaemia, haematuria
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investigations for endometrial cancer
- transvaginal USS (normal endometrial thickness <4mm post-menopause) - pipelle biopsy - hysteroscopy with biopsy
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ovarian cancer
- often presnt late due to non-specific symptoms - >70% present when spread beyond the pelvis
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ovarian cancer types
* Epithelial cell tumours: most common – sub types (serous tumours most common) * Dermoid cysts/germ cell tumours: benign, teratomas (come from germ cells), contain various tissue types, can cause ovarian torsion, can cause raised hCG * Sex cord-stromal tumours: benign or malignant, arise from stoma (connective tissue) or sex cords – several types including Sertoli–Leydig cell tumours and granulosa cell tumours * Metastasis: A Krukenberg tumour refers to a metastasis in the ovary, usually from a gastrointestinal tract cancer (stomach) – signet ring cells on histology
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risk/protective factors for ovarian cancer
Risk Factors – age, BRCA1/2, increased number of ovulations, obesity, smoking Protective Factors – COC, breastfeeding, pregnancy
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presentation of ovarian cancer
– abnormal bloating, early satiety, loss of appetite, pelvic pain, urinary symptoms, weight loss, abdo/pelvic mass, ascites, may press on obturator nerve causing hip/groin pain (NON-SPECIFIC)
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investigations for ovarian cancer
- CA125 blood test (>35 IU/mL is significant), pelvic USS - risk of malignancy index (RMI) - CT (stage), biopsy, paracentesis (ascitic tap to test cells) - <40y need alpha-FP and hCG for germ cell
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causes of raised CA125
tumour marker for epithelial cell ovarian cancer but not very specific – endometriosis, fibroids, adenomyosis, pelvic infection, liver disease, pregnancy
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vulval cancer
- Rarer, 90% are squamous cell carcinomas - age, immunosuppression, HPV, lichen sclerosis (5% with this get vulval cancer) - skin changes - lump/ulcer/pain etc mostly labia majora - biopsy with node biopsy - wide excision, lymph node removal, chemo, radio
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vaginal cancer
mostly squamous cell carcinoma like vulval cancer management may present with dyspareunia
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structural causes of abnormal menstrual bleeding PALM
P – polyps (endometrial or cervical) A – adenomyosis L – leiomyoma (fibroid) M – premalignancy (endometrial hyperplasia), malignancy
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non-structural causes of abnormal menstrual bleeding COEIN
C – systemic coagulopathy (thrombocytopenia, von Willebrand’s disease, leukaemia, warfarin O – ovulatory dysfunction (PCOS, hypothyroidism, Cushing’s, hyper prolactinoma, congenital adrenal hyperplasia) E – primary endometrial disorders (endometritis) I – iatrogenic (contraceptives) N – generally rare causes
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red flag signs for abnormal menstrual bleeding
Suspected cancer – PCB, PMB, pelvic mass, cervix lesion
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intermenstrual bleeding
* ovulation causes spotting in 1-2% * uterine causes: iatrogenic (contraceptives), endometritis, uterine polyps, fibroids, adenomyosis, endometrial cancer * cervical causes: following examination, infection, cervical ectropion, cancer * vaginal causes: infection, cancer
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heavy menstrual bleeding
- >80ml but based on effect of QOL and symptoms - Exclude underlying pathology – anaemia, fibroids, bleeding disorder (will have been heavy bleeding since menarche), cancer - tranexamic acid if no pain, mefenamic acid if pain (NSAID + reduces bleeding), hormonal contraceptives (Mirena)
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postcoital bleeding
Non-menstrual genital tract bleeding immediately or shortly after intercourse Mostly from cervical causes or vaginal atrophy (post menopause)
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causes of postmenopausal bleeding
* Polyps 30% * Submucosal fibroids 20% * Endometrial atrophy 30% * Hyperplasia 10% * Endometrial carcinoma 5-8% * Ovarian, tubal, cervical malignancy 2%
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fibroids + types/symptoms/investigations
- also called leiomyomas - tumour of smooth muscle - affect 40-60%, oestrogen sensitive (grow during cycle and pregnancy) - can be intramural, subserosal, submucosal or pedunculated - often asymptomatic, heavy and prolonged menstrual bleeding, pain, bloating, urinary or bowel symptoms, deep dyspareunia, reduced fertility - hysteroscopy, pelvic USS, MRI before surgery
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management of fibroids
- For fibroids <3cm: o Mirena coil (first line), symptomatic management, COC, cyclical oral progestogens o Endometrial ablation, resection, hysterectomy - Fibroids >3cm: same but Mirena coil can’t be used o Uterine artery embolization, myomectomy, hysterectomy o GnRH agonist (Zoladex) may be used to reduce size before surgery
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red degeneration of fibroids
- ischaemia and infarction when it outgrows its blood supply (mostly in 2nd/3rd trimester of pregnancy) - severe abdo pain, fever, tachycardia, vomiting - rest, fluids and analgesia
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what is endometriosis
Ectopic endometrial tissue (an endometrioma) outside of the uterus
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symptoms of endometriosis
- cyclical dull heavy pain, blood in urine/stools (if in bladder/bowel), adhesions (chronic sharp pain), reduced fertility (adhesions block tubes), deep dyspareunia
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diagnosis of endometriosis
- USS may reveal large endometriomas and chocolate cysts but often unremarkable - laparoscopy gold standard with biopsy
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management of endometriosis
- Initial management: establish diagnosis, education, analgesia, listen to patient - Hormonal: any contraceptive hormones, GnRH agonists such as Zoladex only used short term (stop FSH/LH release) - Surgical: laparoscopy to remove or ablate lesions and adhesiolysis, hysterectomy
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adenomyosis
- Endometrial tissue inside the myometrium of uterus, more common in multiparous women, 10% of women, hormone-dependant so normally resolve after menopause. - Associated with pregnancy complications (infertility, miscarriage, preterm birth, SGA, PROM, malpresentation, CS, PPH - painful/heavy periods, dyspareunia - USS - management varies (tranexamic/mefenamic acid, contraceptives, endometrial ablation, uterine artery embolization, hysterectomy)
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endometrial polyps
- over growth of endometrium extending into uterine cavity - can be precancerous - most postmenopausal, oestrogen sensitive - irregular bleeding, IMB, PMB, infertility - transvaginal USS, hysteroscopy, biopsy - Treatment – watch and wait, hormonal medications, polypectomy during hysteroscopy
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what is an ovarian cyst
- fluid filled sac - functional ovarian cysts related to fluctuating hormones - very common premenopause - postmenopausal cysts more concerning - multiple cysts or 'string of pearls' appearance still need other symptoms to be diagnosed with PCOS
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presentation of ovarian cysts
most asymptomatic, pelvic pain, bloating, fullness, palpable pelvic mass, may be acute pain due to rupture, torsion or haemorrhage
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functional ovarian cysts
- follicular cysts most common - follicle fails to rupture - resolves after a few cycles - corpus luteum cysts - fails to break down, often seen in early pregnancy
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investigations for ovarian cysts
- assessment of red flags - premenopausal with simple ovarian cyst <5cm on USS no further investigations - <40 with complex mass need tumour markers for germ cell tumour
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management of ovarian cysts
- Simple ovarian cysts in premenopausal women: o Less than 5cm cysts - almost always resolve within three cycles. They do not require a follow-up scan. o 5cm to 7cm: Require routine referral to gynaecology and yearly ultrasound monitoring. o More than 7cm: Consider an MRI scan or surgical evaluation - Cysts in premenopausal women need referral to gynae and CA125 - Ovarian cystectomy or oophorectomy in some cases
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Meig's syndrome
* Triad of ovarian fibroma, pleural effusion, ascites * Typically in older women, removal of tumour results in complete resolution of effusion and ascites
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polycystic ovarian syndrome
- common condition causing metabolic and reproductive problems in women - Characteristic features of multiple ovarian cysts, infertility, oligomenorrhea, hyperandrogenism (effects of high testosterone) and insulin resistance (most get diabetes)
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Rotterdam criteria for PCOS diagnosis
Needs at least 2 of – oligoovulation/anovulation, hyperandrogenism (hirsutism (male hair pattern) and acne), polycystic ovaries on USS
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insulin resistance and PCOS
- crucial feature - more insulin produced - promotes release of more androgens (from ovaries and adrenal gland) and suppresses sex hormone-binding globulin (SHBG) production by the liver (normally reduces effects). - high insulin contributes to halting development of follicles - diet, weight loss and exercise can help
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investigations for PCOS
- Raised LH - Raised LH to FSH ratio (high LH compared with FSH) - Raised testosterone - Raised insulin - Normal or raised oestrogen levels - USS >12 cysts in each ovary - oral glucose tolerance test
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management of PCOS
- Reduce associated risks – weight loss (can restore fertility and reduce symptoms), low GI diet, exercise, smoking cessation, antihypertensives, statins (if QRISK >10%) - mirena/ cyclical contraceptives to reduce endometrial cancer - Fertility – weight loss, clomifene, laparoscopic ovarian drilling (multiple punctures in ovary), IVF - hirsutism - COC, topical treatments, laser hair removal
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ovarian torsion
- ovary twists - ischaemia and necrosis if not fixed - usually due to ovarian mass >5cm - acute severe unilateral pelvic pain, gets worse, may be intermittent, nausea. palpable mass - USS (whirlpool sign, oedema), doppler studies (lack of blood flow), laparoscopy - emergency detorsion or oophorectomy - may lose function if delayed or become infected
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Lichen sclerosis
- Chronic autoimmune inflammatory skin condition that presents with patches of shiny, “porcelain-white” skin, commonly on labia, perineum, perianal skin - age 45-60, itching, soreness, skin tightness, superficial dyspareunia, erosions, fissures, Koebner phenomenon (symptoms made worse by friction to skin - porcelain white in colour, shiny, tight, thin, slightly raised, may be papules - symptom management - topical dermovate titrated down gradually, emollients
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what is androgen insensitivity syndrome
- lack of androgen receptors, extra androgens converted into oestrogen resulting in female secondary sexual characteristics - X-linked AR in genetically male (XY) but no response to testosterone so female phenotype externally with testes inside and no upper vagina onwards - infertile, increased risk of testicular cancer - normally raised as female
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presentation of androgen insensitivity syndrome
- in infancy with inguinal hernias containing testes - in puberty with primary amenorrhoea - high LH, high FSH, normal/raises testosterone, raised oestrogen
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management of androgen insensitivity syndrome
- MDT - orchidectomy - prevent testicular cancer - oestrogen therapy - vaginal dilators or surgery to create adequate length
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bicornate uterus
- heart shapes - 2 horns - can be associated with miscarriage, premature birth, malpresentation
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imperforate hymen
* Hymen is fully formed, blocking vaginal opening * May be discovered in infancy or during first menstruations with cyclical pain but no bleeding * Needs surgery to avoid blocking ureters and avoid infection
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transverse vaginal septum
* a septum (wall) forms transversely across the vagina, can be perforate or imperforate * can lead to infertility and pregnancy complications * needs surgery
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vaginal hypoplasia and agenesis
* Vaginal hypoplasia refers to an abnormally small vagina * Vaginal agenesis refers to an absent vagina * Due to failure of the Mullerian duct development * Treat with vaginal dilator over time or surgery
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what is turners syndrome
female has a single X chromosome, making them 45 XO
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features of turners syndrome
- 3 classic features – short stature, webbed neck, widely spaced nipples - High arching palate, downwards sloping eyes with ptosis, broad chest, cubitus valgus (when arm extended the forearms are angled outwards), underdeveloped ovaries, late/incomplete puberty, most women are infertile - associated with autoimmune conditions and recurrent otitis media and UTI
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management of turners syndrome
- GH therapy to prevent short stature - oestrogen and progesterone therapy - fertility treatment monitoring for associated conditions
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Asherman's syndrome
- adhesions form within uterus following damage to basal layer of endometrium (eg after D&C) - lighter/painful periods, infertility, recurrent miscarriage - hysteroscopy with adhesiolysis, recurrence is common
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prolactinoma
- prolactin secreting pituitary tumour - micro <10mm, macro>10mm - causes hypogonadism (decreases oestrogen and testosterone) - Females – irregular/absent periods, milky discharge from nipple, vaginal dryness, acne - Males – erectile dysfunction, decreased body and facial hair, smaller muscles, enlarged breasts - Both – infertility, osteoporosis, loss of libido - Diagnosis – bloods for hormone levels, MRI or CT head, visual field tests - Treatment – dopamine agonists (cabergoline – decrease production of prolactin and decrease size of tumour), surgical removal
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what is the UKMEC criteria
- UK medical eligibility criteria used for contraceptives * UKMEC 1: No restriction in use (minimal risk) * UKMEC 2: Benefits generally outweigh the risks * UKMEC 3: Risks generally outweigh the benefits * UKMEC 4: Unacceptable risk (typically this means the method is contraindicated)
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risk factors for COC (UKMEC 4)
uncontrolled HTN, migraine with aura, VTE history, age >35 and smoking, surgery with prolonged immobility, CVD, stroke, liver cirrhosis or tumours, SLE, clotting abnormalities
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Fraser criteria for contraception under 16y
- can be prescribed if: she understands advice, cant be persuaded to tell parents, likely to continue being sexually active, likely to mentally or physically suffer without, best interest
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pretesticular causes of male infertility
anything that reduced testosterone – pathology of pituitary or hypothalamus, stress, chronic conditions, Kallman Syndrome
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testicular causes of male infertility
* From damage – mumps, undescended testes, trauma, radiotherapy, chemotherapy, cancer * Genetic conditions – Klinefelter syndrome, Y chromosome deletions, Sertoli cell-only syndrome, anorchia (absent testes)
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post testicular causes of male infertility
damage from trauma, ejaculatory duct obstruction, retrograde ejaculation, scarring from infection, Young’s syndrome
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Klinefelter syndrome
* Males born with XXY, often not diagnosed until adulthood * Small testes, reduced muscle mass/facial hair, enlarged breast tissue * Many complications/related conditions * Treatment of symptoms, testosterone replacement therapy, fertility treatment
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IVF process
- 25-30% success rate - supress natural cycle (GnRH agonists or antagonists) – ovarian stimulation (FSH SC for 10-14 days then hCG given then after 36h oocytes collected) – oocyte collection (needle through vagina, US guided) – insemination or intracytoplasmic sperm injection – embryo culture (until blastocysts, day 5) – embryo transfer (after 2-5 days, one/ 2 in older woman)
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urge incontinence/overactive bladder
* overactivity of the detrusor muscle of the bladder * suddenly feeling the urge to pass urine, having to rush to the bathroom and not arriving before urination occurs * significant impact of QOL
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stress incontinence
- weakness of the pelvic floor and sphincter muscles allowing urine to leak during times of increased abdominal pressure
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investigations for urinary incontinence
- bladder diary - urine dipstick - post-void residual bladder scan - urodynamic testing if not responding to treatment
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management of stress incontinence
- lifestyle changes - supervised pelvic floor exercises for >3m before surgery -surgery: tension-free vaginal tape, autologous sling, colposuspension, intramural urethral bulking - duloxetine (SNRI) when surgery is less preferred
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management of urge incontinence
- bladder retraining - anticholinergics (oxybutynin) - more invasive procedures: Botox A injections, sacral nerve stimulation etc
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vault prolapse
after hysterectomy, vaginal vault descends
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rectocele
defect in posterior vaginal wall so rectum prolapses forwards, associated with constipation, can develop faecal loading leading to constipation and urinary retention, may feel lump in vagina
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cystocele
defect in anterior vaginal wall, bladder prolapse into vagina, prolapse of urethra (urethrocele), both (cystourethrocele)
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presentation of pelvic organ prolapse
- dragging or heavy sensation - urinary symptoms - bowel symptoms - sexual dysfunction - lump or mass in vagina
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grading system for pelvic organ prolapse
- pelvic organ prolapse quantification (POP-Q) system * Grade 0: Normal * Grade 1: The lowest part is more than 1cm above the introitus * Grade 2: The lowest part is within 1cm of the introitus (above or below) * Grade 3: The lowest part is more than 1cm below the introitus, but not fully descended * Grade 4: Full descent with eversion of the vagina
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management of prolapse
- conservative - physio, lifestyle, oestrogen cream - vaginal pessary - hysterectomy
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STD investigations
- Everyone – bloods to check for HIV, Syphilis and Hep B or C - Males – urine sample (chlamydia, gonorrhoea, and mycoplasma), possible swabs (throat, penis, and anal canal) - Females – high vaginal swab o Triple swab:  1 (HVS) – TV, BV, candida  2 (ECS) – GC  3 (chlamydia)
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thrush/candidiasis
- yeast infection with candida (most common candida albicans) - thick white discharge, no smell, irritation - vaginal pH (<4.5 suggests), charcoal swab with microscopy - antifungal (clotrimazole) cream/pessary, fluconazole oral antifungals if severe
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Bacterial vaginosis
- overgrowth of anaerobic bacteria caused by loss of lactobacilli (normally produce lactic acid to keep pH <4.5) - Gardnerella vaginalis most common - fishy-smelling watery grey/white discharge - charcoal swab for microscopy - asymptomatic don't need treatment - metronidazole oral/vaginal (no alcohol) - education of female hygiene - can cause complications in pregnancy
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chlamydia
- gram negative intracellular bacteria - can cause infertility - national screening programme - test <25 annually/aftre new partner, retest after 3m if + - charcoal swabs for microscopy/culture/sensitivities, nucleic acid amplification test (NAAT) - abnormal discharge, dyspareunia, LUTS, reactive arthritis - doxy 100mg twice a day for 7 days (azithromycin in pregnancy) - abstain from sex for 7d, refer to GUM for contact tracing
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Lymphogranuloma Venereum
* condition affecting the lymphoid tissue around the site of infection with chlamydia, most common in men who have sex with men * primary stage – painless ulcer * secondary stage – lymphadenitis * tertiary stage – inflammation of rectum (proctitis) – pain, change in bowel habit, tenesmus, discharge * Doxycycline 100mg twice daily for 21 days
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chlamydial conjunctivitis
- usually when genital fluid encounters the eye - chronic erythema, irritation and discharge lasting more than two weeks, most are unilateral
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gonorrhoea
- gram-negative diplococcus infecting mucous membranes with columnar epithelium (endocervix, urethra, rectum, conjunctiva, pharynx) - high level of abx resistance (ciprofloxacin, azithromycin)
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presentation of gonorrhoea
* Odourless purulent discharge, possibly green or yellow, dysuria, pelvic or testicular pain * Gonococcal conjunctivitis in neonate if infected mother (medical emergency, related to sepsis, perforation of the eye, and blindness)
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diagnosis of gonorrhoea
NAAT diagnoses but need charcoal swab for culture and sensitivities
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Management of gonorrhoea
- refer to GUM for treatment and contact tracing - abx depends on sensitivities o 1 dose IM ceftriaxone 1g if the sensitivities are NOT known o 1dose of oral ciprofloxacin 500mg if the sensitivities ARE known - Follow up test of cure – NATT if asymptomatic, cultures if symptomatic
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disseminated gonococcal infection
*Complication of untreated infection – bacteria spreads to skin and joints *Skin lesions, polyarthralgia, migratory polyarthritis (moves between joints), tenosynovitis, systemic symptoms
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mycoplasma Genitalium
- bacteria causing non-gonococcal urethritis - STI - presents similar to chlamydia but with urethritis - NAAT - doxy 100mg BDS for 7d then azithromycin - follow up test of cure
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causes of PID
*Most from STI – gonorrhoea, chlamydia, mycoplasma genitalium *Non-STI – BV, haemophilus influenza, E.coli
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presentation of PID
* Pelvic pain, abnormal discharge or bleeding, dyspareunia, fever, dysuria * On examination – pelvic tenderness, cervical motion tenderness (cervical excitation), cervicitis, purulent discharge
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investigations for PID
- full STI screen - High vaginal swab for BV, candidiasis, trichomoniasis - Microscopy to look for pus cells - Pregnancy test to exclude ectopic - Inflammatory markers raised in PID
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management of PID
- treat any infections (GUM) - 1 dose IM ceftriaxone 1g (cover gonorrhoea) - Doxycycline 100mg BDS for 14 days (to cover chlamydia and Mycoplasma genitalium) - Metronidazole 400mg BDS for 14 days (to cover anaerobes such as Gardnerella vaginalis) - may need admission if severe or pregnant
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Fitz-hugh-curtis syndrome
- Complication of PID, inflammation and infection of the liver capsule (Glisson’s capsule), leading to adhesions between the liver and peritoneum - Bacteria can spread via peritoneal cavity, lymphatics or blood - Right upper quadrant pain (can have shoulder tip pain) - Laparoscopy to visualise and adhesiolysis to treat adhesions
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trichomoniasis
- trichomoniasis vaginalis - sexually transmitted parasite - protozoan (single celled organism with flagella) - urethra of men and urethra/vagina of women - can increase risks of other infections and pregnancy complications
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presentation of trichomoniasis
* 50% of cases are asymptomatic * Vaginal discharge (frothy, yellow-green), dysuria, itching, dyspareunia, balanitis (inflammation of gland penis) * On examination – strawberry cervix (colpitis macularis) * Raised vaginal pH
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diagnosis of trichomoniasis
* Can be confirmed on charcoal swab with microscopy – taken in posterior fornix or urethra/first-catch urine
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management of trichomoniasis
* Referral to GUM * Metronidazole
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genital herpes
HSV - both cold sores (herpes labialis) and genital herpes, 2 types HSV-1 HSV-2 - after infection it becomes latent in sacral nerve ganglia
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presentation of genital herpes
* Ulcers or blistering lesions affecting the genital area * Neuropathic type pain (tingling, burning or shooting) * Flu-like symptoms (e.g. fatigue and headaches) * Dysuria (painful urination) * Inguinal lymphadenopathy * First infection normally lasts 3 weeks and is the worst
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management of genital herpes
- diagnosis via viral PCR - Referral to GUM - Aciclovir - Methods to ease symptoms (paracetamol, loose clothing, topical lidocaine etc.)
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pregnancy and genital herpes
- risk of neonatal HSV (high mortality) - treatment with aciclovir for first infection then prophylactic aciclovir from 28w, may need CS if symptomatic - if latent then may not need aciclovir
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HIV
RNA retrovirus HIV-1 most common, HIV2 rare outside west africa
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AIDS defining illnesses
- when CD4 count has dropped significantly = opportunistic infections and malignancy - Kaposi’s sarcoma, Pneumocystis jirovecii pneumonia (PCP), Cytomegalovirus infection, Candidiasis (oesophageal or bronchial), Lymphomas, TB
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screening for HIV
- test anyone in hospital with infectious disease - test everyone with risk factors - can take up to 3m for abs to develop so may need repeat test - need verbal consent documented
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tests for HIV
* antibody testing – blood test * p24 antigen (specific HIV antigen in blood) – can give positive result earlier in infection * PCR testing for HIV RNA (viral load)
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treatment for HIV
- specialist HIV, infectious disease or GUM centres - Combination of antiretroviral therapy (ART) medications offered to everyone with a HIV diagnosis - starting regime of two NRTIs (e.g. tenofovir and emtricitabine) plus a third agent - aim to have normal CD4 count and undetectable viral load - prophylactic co-trimoxazole if low CD4 count
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preventing HIV transmission during birth
o Normal vaginal delivery if viral load < 50 copies / ml o CS if > 50 copies/ ml and in all women with > 400 copies / ml o IV zidovudine should be given during the caesarean if the viral load is unknown or there are > 10000 copies / ml - low risk babies given 4w zidovudine, high risk given 3 drugs
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breastfeeding and HIV
can be transmitted in breast milk even if viral load undetectable
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post-exposure prophylaxis for HIV
- start within 72h - ART tx - truvada and raltegravir for 28d
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syphilis
called Treponema pallidum – spirochete, gets in through skin or mucous membranes, mainly a sexually transmitted infection, incubation period of 21 days
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primary syphilis
- painless ulcer (chancre) 3-8w - local lymphadenopathy
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secondary syphilis
lasts 3-12w then into latent phase - systemic symptoms - o Maculopapular rash o Condylomata lata (grey wart-like lesions around the genitals and anus) o Low-grade fever o Lymphadenopathy o Alopecia (localised hair loss) o Oral lesions
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tertiary syphilis
- many years after infection it can affect many organs o Gummatous lesions (gummas are granulomatous lesions that can affect the skin, organs and bones) o Aortic aneurysms o Neurosyphilis (headache, dementia, altered behaviour, demyelination, ocular syphilis, paralysis, sensory impairment)
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diagnosis of syphilis
*Antibody testing – screening *Dark field microscopy and PCR can confirm presence of T.pallidum
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management of syphilis
- specialist or GUM service - contact tracing, full STI test - Single deep IM dose of benzathine benzylpenicillin
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genital warts
- HPV affecting moist tissues of genitals (flesh coloured bumps or cauliflower-like) - Cream: imiquimod - Laser removal - Freezing therapy – liquid nitrogen
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risk factors for breast cancer
female, increased oestrogen exposure, more dense/glandular breast tissue, obesity, smoking, family history, COC (small risk then reverses after 10 years), combined HRT?
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BRCA genes
- tumour suppressor genes - BRCA1 gene chromosome 17- 70% get breast cancer by 80, 50% get ovarian, increased risk of bowel and prostate - BRCA2 on chromosome 13 – 60% get breast cancer, 20% get ovarian
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types of breast cancer - ductal carcinoma in situ
- pre/cancerous epithelial cells of breast ducts - localised to single area - often found at mammogram - 30% become invasive - good prognosis with full excision and adjuvant tx
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types of BC - lobular carcinoma in situ
- pre-cancerous - pre-menopausal - usually asymptomatic and undetectable on mammogram - increased risk of bc in future - close monitoring - 6m examination, 1y mammogram
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types of bc - invasive ductal carcinoma
- from cells in breast ducts - 80% of invasive cancers - seen on mammogram
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types of breast cancer - invasive lobular carcinoma
- 10% of invasive bc - from cells in breast lobules - not always visible on mammogram
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types of bc - inflammatory bc
- 1-3% of bc - presents similarly to breast abscess or mastitis (swollen, warm, tender, peau d’orange), doesn’t respond to abx - worse prognosis
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types of bc - Paget's disease of the nipple
Looks like eczema on nipple/areola, erythematous/scaly rash, indicated breast cancer involving the nipple, may represent DCIS or invasive breast cancer
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breast cancer screening
*NHS screening – mammogram every 3y for women between 50-70y *1 in 100 diagnosed with breast cancer from screening
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high risk patients for bc
* First degree relative with: bc under 40y/o, or male bc, or bilateral bc under 50, or two with bc * Need genetic counselling and pre-test counselling before genetic tests * Annual mammogram (potentially starting at 30) * Chemoprevention – tamoxifen (premenopause), anastrozole (postmenopause) * Bilateral mastectomy or oophorectomy
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presentation of bc
* Lumps that are hard, irregular, painless or fixed in place * Lumps may be tethered to the skin or the chest wall * Nipple retraction * Skin dimpling or oedema (peau d’orange) * Lymphadenopathy, particularly in the axilla
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triple diagnostic test for bc
- clinical assessment - imaging - USS (younger women), mammogram , MRI - biopsy - fine needle aspiration or core biopsy
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lymph node biopsy for bc
* Ultra-sound guided biopsy * Sentinel lymph node biopsy – during breast surgery, isotope contract and blue dye injected into tumour area then travels to lymph node then can biopsy
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breast cancer receptors
- gene expression profiling * Oestrogen receptors (ER) * Progesterone receptors (PR) * Human epidermal growth factor (HER2)
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most common metastasis for bc
lungs, liver, bones, brain
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staging used for BC
- TNM - Nottingham score - prognostic
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treatment for bc
- surgery: mastectomy, lumpectomy+adjuvant therapy, axillary clearance of lymph nodes - radiotherapy: can cause damage to breast tissue so only one round done - chemo: neoadjuvant (shrink), adjuvant and treatment of metastatic/recurrent bc - hormone therapy: if ER+ tamoxifen and aromatase - targeted treatment - Trastuzumab (Herceptin) and Pertuzumab (Perjeta) – monoclonal antibodies that target HER2 receptor
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benign breast lumps - fibroadenoma
* common benign tumours of stromal/epithelial breast duct tissue * typically small and mobile, more common between 20-40 because they respond to the female hormones * painless, smooth, round, well circumscribed, firm, mobile, usually up to 3cm
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benign breast lumps - fibrocystic breast changes
- variation of normal, fluctuate with cycle - tissues respond to sex hormones and become fibrous and cystic - manage symptoms
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benign breast lumps - breast cysts
* benign, individual, fluid-filled lumps – most common cause of lumps between 30-50 * can be painful and fluctuate in size over the menstrual cycle * smooth, well circumscribed, mobile, possibly fluctuant * often need further assessment to rule out cancer, may slightly increase risk * aspiration can ease symptoms
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benign breast lumps - fat necrosis
- localised degeneration and scarring of fat tissue - from trauma, radiation, inflammatory reaction - may need biopsy to rule out bc - painless, firm, irregular, fixed, possible skin dimpling or nipple inversion - resolve spontaneously or surgery
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benign breast lumps - galactocele
occur after stopping breastfeeding, breast milk filled cysts from lactiferous duct blockage, usually resolve without intervention
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benign breast lumps - Phyllodes tumour
* rare tumours of the connective tissue (stroma) of the breast, mostly in 40-50s * large and fast growing * can be benign (~50%), borderline (~25%) or malignant (~25%).