TO DO WOMENS HEALTH Flashcards
(225 cards)
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
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
3
Q
MISCARRIAGE
What is an inevitable miscarriage?
A
- Miscarriage will occur
- Heavy PV bleed with clots + crampy abdo pain with OPEN cervical os (1 finger)
- POC not passed
- TVS = intrauterine gestation sac, foetus may be alive but miscarriage imminent
4
Q
MISCARRIAGE
What is the medical management of a miscarriage?
What is the follow up?
A
- PV/PO synthetic prostaglandin MISOPROSTOL
- Contact HCP if no bleeding in 24h
- Urinary beta-hCG 3w after to exclude ectopic or molar
5
Q
TERMINATING PREGNANCY
What is the medical management of abortion?
A
- More appropriate in earlier pregnancy, <24w, <10w can be done at home
- MIFEPRISTONE (anti-progesterone) to halt pregnancy + relax cervix
- MISOPROSTOL (prostaglandin analogue) 24-48h after for contractions
6
Q
TERMINATING PREGNANCY
What is done before surgical management of abortion?
A
- Cervical priming with mifepristone, misoprostol or osmotic dilators (>14w insert into cervix + gradually expand as absorb fluid to open cervical canal)
7
Q
HYPEREMESIS
What is the diagnostic triad for hyperemesis gravidarum?
A
Triad –
- >5% weight loss compared to before pregnancy
- Dehydration
- Electrolyte imbalance
8
Q
HYPEREMESIS
What would warrant hospital or EPAU admission?
A
- Unable to tolerate PO antiemetics or fluids
- > 5% weight loss compared to before pregnancy
- Ketones present in dipstick (++ significant)
9
Q
HYPEREMESIS
What is the inpatient management of hyperemesis gravidarum?
A
- Monitor U+Es
- NBM until tolerate PO = IV fluids + anti-emetics
- Vitamin supplements (incl. thiamine), may need artificial nutrition to prevent Wenicke-Korsakoff
- Thromboprophylaxis with TED stockings + LMWH
- Small + frequent meals when eating allowed
10
Q
HYPEREMESIS
What is the community management of hyperemesis gravidarum?
A
- 1st line antiemetic = promethazine or cyclizine (anti-histamines)
- 2nd line = ondansetron (5-HT3 antagonist) or metoclopramide (dopamine antagonist)
11
Q
ANTENATAL APPTS
What routine care is given at 28w?
A
- BP, urine dipstick, SFH
- OGTT if risk factors for GDM
- Second screen for anaemia (FBC), blood group + rhesus status
- First dose of anti-D prophylaxis if Rh-ve
12
Q
ANTENATAL SCREENING
What screening is offered in early pregnancy and when?
A
Combined test (11–13+6w) –
- Nuchal translucency (thickness of back of foetus’ neck on USS)
- Beta-hCG
- Pregnancy associated plasma protein-A (PAPP-A)
13
Q
ANTENATAL SCREENING
What screening is offered if the mother is too late for the combined test and when?
A
Triple or quadruple test 15–20w but only tests for Down’s syndrome –
- Beta-hCG
- Alpha-fetoprotein
- Oestriol
- Inhibin (quadruple)
14
Q
ANTENATAL SCREENING
What results indicate higher risk for…
i) beta-HCG?
ii) AFP?
iii) oestriol?
iv) inhibin?
A
i) Higher result
ii) Lower result
iii) Lower result
iv) Higher result
15
Q
APH
What are some generic investigations for APH?
A
- Exclude placenta praevia with USS
- Kleihauer test to confirm transplacental blood loss from foetus>mother
16
Q
PLACENTA PRAEVIA
What are some risk factors for placenta praevia?
A
- Embryos more likely to implant on lower segment scar from previous c-section
- Multiple pregnancy
- Multiparity
- Previous praevia
- Assisted conception
17
Q
PLACENTAL ABRUPTION
What are the major risk factors for placental abruption?
What are some other risk factors?
A
- IUGR, pre-eclampsia or pre-existing HTN, maternal smoking + previous abruption
- Cocaine use, multiple pregnancy or high parity, trauma
18
Q
PLACENTAL ABRUPTION
What is the general management of placental abruption?
A
- Mum + foetus stable at <36w then admit + observe carefully, induce after 36w with amniotomy aiming for vaginal delivery, steroids if <34w
- Anti-D if Rh-ve
19
Q
ADHERED PLACENTA
What are the different types of morbidly adhered placenta?
A
- Accreta = placenta invades into superficial myometrium
- Increta = placenta invades deeper through the myometrium
- Percreta = placenta invades through myometrium, into nearby organs of abdomen (bladder, bowel)
20
Q
ADHERED PLACENTA
What are some risk factors for a morbidly adhered placenta?
A
- Previous c-sections (placenta attaches to site)
- Myomectomy
- Surgical TOP
21
Q
VASA PRAEVIA
What are some risk factors for vasa praevia?
A
- Placenta praevia
- Multiple pregnancy
- IVF pregnancy
- Bilobed placentas
22
Q
PRE-ECLAMPSIA
What is the normal physiology of the placenta?
A
- Spiral arteries dilate + develop into large utero-placental arteries, supplying lots of blood to the endometrium > placenta + foetus
23
Q
PRE-ECLAMPSIA
What is the pathophysiology of pre-eclampsia?
A
- Spiral arteries do not remodel + dilate but become fibrous so utero-placental arteries deliver less blood > placental ischaemia
24
Q
PRE-ECLAMPSIA
What is the result of placental ischaemia?
A
- Pro-inflammatory protein + thromboplastin release leads to endothelial damage > vasoconstriction, clotting dysfunction + increased vascular permeability
- Ultimately leads to poor renal perfusion > RAAS activation > HTN, proteinuria ± oedema > pre-eclampsia + eclampsia (if continues)
25
PRE-ECLAMPSIA
What are the...
i) high risk
ii) moderate risk
factors for pre-eclampsia?
i) Pre-existing HTN, previous pre-eclampsia, CKD, autoimmune (SLE, T1DM)
ii) Nulliparity, multiple pregnancy, >10y pregnancy interval, FHx, >40y, BMI >35kg/m^2
26
PRE-ECLAMPSIA
What are the 2 main causes of symptoms in pre-eclampsia?
- Local areas of vasospasm leading to hypoperfusion
- Oedema due to increased vascular permeability + hypoproteinaemia
27
PRE-ECLAMPSIA
What symptoms are caused by local areas of vasospasm and what area is affected?
Renal = glomerular damage (low GFR) –
- Oliguria + proteinuria
Retinal –
- Visual disturbances (blurred, flashing lights, scotoma)
Liver = injury + swelling stretches liver capsule –
- RUQ or epigastric pain
28
PRE-ECLAMPSIA
What symptoms are caused by oedema?
- Face, hands + legs (generalised)
- SOB + cough (pulmonary)
- Headaches, confusion + seizures in eclampsia (cerebral)
29
PRE-ECLAMPSIA
What are the signs of pre-eclampsia?
- Raised BP + proteinuria are hallmarks
- Rapid weight gain, RUQ tenderness
- Ankle clonus (brisk reflexes normal in pregnancy but not clonus)
- Papilloedema if severe
30
ECLAMPSIA
What is the management of eclampsia?
IV magnesium sulfate to prevent + treat seizures –
- Reduces DIC risk as reduced platelet aggregation
- Continue 24h after last seizure or delivery
Treat HTN with labetalol 1st line or nifedipine
Stabilise mum and delivery baby
31
HELLP
How does HELLP syndrome present?
➢ Nausea/vomiting
➢ Hypertension
➢ Brisk tendon reflexes
➢ RUQ/Epigastric pain
➢ General malaise/headache
➢ Oedema/bleeding
➢ Visual problems, jaundice
32
PRE-ECLAMPSIA
What medical treatment can be given for pre-eclampsia?
Treat HTN with –
- PO Labetalol first line (can use IV if severe + inpatient)
- PO nifedipine (used if asthmatic)
- Hydralazine too
- ACEi = CONTRAINDICTAED
33
PRE-ECLAMPSIA
What is the management of pre-eclampsia during delivery?
- Regular investigations (BP, urinalysis, bloods, CTG, fluid balance chart (restrict if severe)
- BP control (IV labetalol first line of nifedipine if asthmatic)
- IV magnesium sulfate prophylaxis during labour + 24h after
34
IUGR
What are some placental causes of IUGR?
- Abnormal trophoblast invasion (pre-eclampsia, placenta accreta)
- Infarction, abruption, location (praevia)
35
IUGR
What are some maternal causes of IUGR?
- Chronic disease (HTN, cardiac, CKD)
- Substance abuse (cocaine, alcohol) smoking, previous SGA baby
- Autoimmune
- Low socioeconomic status
- >40
36
IUGR
What are some foetal causes of IUGR?
- Genetic abnormalities (trisomies 13/18/21, Turner's)
- Congenital infections (TORCH)
- Multiple pregnancy
37
IUGR
What are some complications of IUGR?
- Hypoglycaemia
- Risk of necrotising enterocolitis
- Neonatal jaundice
- Hypothermia
- Respiratory issues
- Long-term sequelae include T2DM, HTN, obesity, behavioural problems, CP
38
IUGR
What are the investigations for IUGR?
- BP + urine dipstick (?pre-eclampsia)
- Karyotyping (?foetal)
- Infection screen, TORCH (?infection)
39
IUGR
When would you be concerned about IUGR?
What would you do?
- 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
40
MULTIPLE PREGNANCY
What is the management of multiple pregnancies?
- Steroids if <34w
- Monochorionic/amniotic twins = elective c-section 32-34w
- Diamniotic twins = 37–38w, vaginal if presenting twin cephalic but may need c-section for second
41
OLIGOHYDRAMNIOS
What are some causes of oligohydramnios?
- 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
42
OLIGOHYDRAMNIOS
What are some complications of oligohydramnios?
- 2nd trimester = poor prognosis due to PPROM leading to premature delivery + pulmonary hypoplasia > resp distress
- Muscle contractures as amniotic fluid allows foetal to move limbs in utero
43
POLYHYDRAMNIOS
What are the causes of polyhydramnios?
- 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)
44
RHESUS DISEASE
What is the pathophysiology of rhesus disease in the first pregnancy?
- Rh-ve woman exposed to Rh+ve foetal blood, her immune system recognises as foreign + produce antibodies against rhesus D (sensitisation)
- Usually no issues in 1st pregnancy as IgM produced that cannot cross placenta
45
RHESUS DISEASE
What is the pathophysiology of rhesus disease in subsequent pregnancies?
- Memory cells produce IgG which can cross placenta so if Rh+ve foetus will attack leading to haemolysis (haemolytic disease of newborn) with jaundice + hydrops fetalis (abnormal accumulation of fluid)
46
RHESUS DISEASE
What are some investigations for rhesus disease?
- 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
47
GESTATIONAL DIABETES
What is the pathophysiology of GDM?
- 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
48
GESTATIONAL DIABETES
What are the maternal risks of GDM?
- Pre-eclampsia
- DKA or hypos
- UTIs
- IHD
- Nephropathy, retinopathy
49
GESTATIONAL DIABETES
What is the management of GDM?
- Fasting glucose <7 = lifestyle (low GI foods, exercise) > metformin after 1-2w if targets not met
- Fasting glucose ≥7 = insulin ± metformin
- Fasting glucose ≥6 + macrosomia or other complications = insulin
- Glibenclamide if cannot tolerate metformin or decline insulin
50
VTE IN PREGNANCY
What are the...
i) high
ii) intermediate
risk factors of VTE?
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
51
VTE IN PREGNANCY
How do you manage VTE risk in pregnancy?
- Risk assessment at booking, antenatal admissions + postnatally
- Antenatal: LMWH from 28w if increased risk or ASAP if high risk
- Postnatal: LMWH for 10d if increased risk or 6w if high risk
- TED stockings
- Low risk Mx = mobilise early, hydration
52
OBSTETRIC CHOLESTASIS
What is the clinical presentation of obstetric cholestasis?
- Typically later in pregnancy (3rd trimester)
- Itchy skin (palms of hands + soles of feet) but with NO rash – WORSE at night
- Jaundice, pale greasy stools + dark urine less common
53
OBSTETRIC CHOLESTASIS
What are the investigations for obstetric cholestasis?
- Clotting screen (prothrombin time) deranged
- Abnormal LFTs + raised bile acids (ALT, AST, GGT + bilirubin raised, ALP too but that is normal in pregnancy), monitor LFTs weekly
54
OBSTETRIC CHOLESTASIS
What is the management of obstetric cholestasis?
- Ursodeoxycolic acid first line to improve LFTs + bile acids
- Induce labour at 37–38w to reduce stillbirth risk
- Vitamin K supplementation
- Emollients (calamine lotion to sooth skin)
- Antihistamines to help sleep
55
GROUP B STREP
What is Group B strep (GBS) infection?
- Infection caused by Strep agalactiae
56
VARICELLA ZOSTER
What is the management of chickenpox exposure in pregnancy?
- 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
57
VARICELLA ZOSTER
What is the management of chickenpox infection in pregnancy?
- PO aciclovir if ≥20w + presents within 24h of rash onset
- <20w then consider
58
PROM
What are some risk factors for (P)PROM?
- Previous PROM/preterm
- Smoking
- Polyhydramnios
- Amniocentesis
59
PROM
What are some investigations for PROM?
- 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)
60
PROM
What is the management of PPROM?
- 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)
61
STAGES OF LABOUR
What are 7 important hormones in labour?
- Prostaglandins
- Oxytocin
- Oestrogen
- Beta-endorphins
- Adrenaline
- Prolactin
- Relaxin
62
STAGES OF LABOUR
What is the first stage of labour?
How is it further divided?
- From onset of labour (true contractions) until the cervix is fully dilated
- Latent phase = from 0–3cm dilation
- Active phase = from 3–10cm
63
STAGES OF LABOUR
What is the second stage of labour?
How is it further divided?
- From full dilation to delivery of the foetus
- Passive stage: complete dilation but no pushing (often 1 hour)
- Active stage: maternal pushing until delivery
64
STAGES OF LABOUR
What is considered a delay in the active second stage of labour?
What does success depend on?
- >2h in nulliparous, 1h in multiparous
- 3Ps (power, passenger + passage [?Psyche of mum])
65
STAGES OF LABOUR
What are the parts of the APGAR score?
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
66
STAGES OF LABOUR
What are the 6 cardinal movements of labour?
- Engagement + descent
- Flexion
- Internal rotation
- Extension (crowning)
- Restitution/external rotation
- Expulsion
67
STAGES OF LABOUR
What position is the foetal head during engagement and descent?
- Occiput transverse
68
FAILURE TO PROGRESS
What may be calculated when considering inducing labour?
What does it calculate?
- Bishop score = used to calculate how likely spontaneous labour is to occur
- Score <5 = unripe cervix (less likely for induction success)
- Score >9 = favourable cervix ready for labour or induction
69
FAILURE TO PROGRESS
What are the components of the Bishop score?
- Cervical dilation – <1cm (0), 1-2 (1), 3-4 (2), >5cm (3)
- Cervical consistency – firm (0), intermediate (1), soft (2)
- Cervical effacement – <30% (0), 40-50 (1), 60-70 (2), 80% (3)
- Cervical position – posterior (0), intermediate (1), anterior (2)
- Foetal station – –3 (0), -2 (1), -1/0 (2), ≥1 (3)
70
FAILURE TO PROGRESS
What are some methods of inducing labour?
- Membrane sweep
- Prostaglandin E2 (PGE2) pessary or gel like dinoprostone
- Cervical ripening balloon (gently inflates + dilates cervix)
- Amniotomy if not ruptured already
- Oxytocin analogue (syntocinon) infusion to cause uterine contractions
71
FAILURE TO PROGRESS
What are some indications and contraindications for inducing labour?
- PROM, IUGR, pre-eclampsia, obstetric cholestasis
- Severe degree of placenta praevia, transverse foetal lie, severe cephalopelvic disproportion, low Bishop score
72
FAILURE TO PROGRESS
In terms of 'passenger' in failure to progress, what is important about position?
- Refers to foetal head position on VE
- Anterior/posterior fontanelles as landmarks, OA ideal
- If OP at delivery means head is at posterior quadrant of pelvis requiring greater rotation which can prolong labour
73
FAILURE TO PROGRESS
How would you manage failure to progress in the first stage of labour?
- PGE2 if low bishop score as if not cannot induce
- Oxytocin infusion ± amniotomy (if membranes not ruptured) > reassess in 2h
- CTG with foetal blood sample if concerns, consider c-section if doesn't help
74
FAILURE TO PROGRESS
How would you manage failure to progress in the third stage of labour?
What are the indications for management?
- 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)
75
BREECH
What are some causes/risk factors for breech presentation?
- 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
76
BREECH
What are the 3 types of breech presentation?
- Extended (Frank) = most common, hips flexed, both legs extended with feet by head, buttocks presenting
- Flexed (Complete) = hips + knees flexed so buttocks + feet presenting (Cannonballing)
- Footling = one leg flexed, one extended, foot hanging through cervix
77
CTG
What are the indications for a continuous cardiotocography (CTG)?
- During labour for every woman
- High risk pregnancies
- Pyrexia (?chorioamnionitis)
- Severe HTN ≥160/110
- Oxytocin use
- Fresh bleeding
78
CTG
How do you interpret a CTG?
Dr C Bravado –
- Dr = define risk (high risk = continuous
- C = contractions (bottom trace shows frequency)
- Bra = baseline rate
- V = variability
- A = accelerations
- D = decelerations
- O = overall assessment
79
CORD PROLAPSE
What are some risk factors for cord prolapse?
- Prematurity
- Polyhydramnios
- Long umbilical cord
- Malpresentation (Footling breech + transverse lie)
- Multiparity + multiple pregnancy
- Placenta praevia
80
CORD PROLAPSE
What is the management of cord prolapse?
- 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
81
SHOULDER DYSTOCIA
What are some risk factors for shoulder dystocia?
- Macrosomia
- Maternal DM
- High maternal BMI
- Cephalopelvic disproportion
- Post-maturity
- Previous shoulder dystocia
82
SHOULDER DYSTOCIA
Explain what is the result of...
i) erb's palsy?
ii) clavicle fracture?
i) Injury of C5/6 nerves causing paralysis of arm, looks limp, waiters tip position
ii) Painful movements, shoulder asymmetry
83
SHOULDER DYSTOCIA
What is the management of shoulder dystocia?
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)
84
INSTRUMENTAL DELIVERY
What are the main risks of ventouse delivery?
- Cephalohaematoma = collection of blood between periosteum + skull from damaged blood vessels, does not cross suture lines, presents hours after
- Caput Succedaneum = Crosses Sutures, diffuse oedema outside periosteum due to pressure to a specific area of scalp, resolve in few days, conehead present at birth
85
INSTRUMENTAL DELIVERY
What are some maternal consequences of instrumental delivery?
- Infection (co-amox stat)
- PPH
- Episiotomy
- Tears
- Incontinence
86
C-SECTION
What are the different categories of c-section?
- 1 = immediate threat to life of mother/baby. Decision>delivery time = 30m
- 2 = not imminent threat to life but c-section required urgently due to compromise. Decision>Delivery time = 75m
- 3 = c-section required but both stable
- 4 = elective section
87
PERINEAL TEARS
What is the classification of perineal tears?
- 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
88
PERINEAL TEARS
How are third degree tears further classified?
- 3A = <50% of external anal sphincter thickness torn
- 3B = >50% of EAS thickness torn
- 3C = EAS + internal anal sphincter torn
89
PPH
What is a primary postpartum haemorrhage (PPH)?
Primary = loss of >500ml blood in the first 24h after delivery
- Minor = 500–1000ml estimated blood loss
- Major = >1000ml, clinically in shock
90
PPH
What are the primary causes of PPH?
Primary (4Ts) –
- Tone (uterine atony = most common)
- Trauma (perineal tear)
- Tissue (retained products)
- Thrombin (clotting issue e.g. DIC in pre-eclampsia)
91
PPH
What are some preventative measures to reduce risk and consequences of PPH?
- Treat anaemia during antenatal period
- Empty bladder (?catheter) as full bladder reduces uterine contractions
- Active Mx of third stage (IM oxytocin)
- IV TXA during c-section in third stage of labour if high risk
92
PPH
What is the role of medical management in PPH?
What is the medical management of PPH?
- All stimulate uterine contractions
- IV syntocinon
- IV/IM ergometrine, C/I in HTN as vasoconstrictor (can combine with syntocinon as syntometrine)
- IM carboprost, caution in asthma (prostaglandin analogue)
- Sublingual misoprostol (prostaglandin analogue)
93
PPH
After failed medical management, what is the surgical management of PPH?
- Intrauterine balloon tamponade (1st line in uterine atony)
- B-lynch sutures (suture around uterus to compress it)
- Internal iliac/uterine artery ligation (reduces blood flow to stop bleeding)
- Hysterectomy as last resort (may save life)
94
HYPEREMESIS
What are some associations of hyperemesis gravidarum?
- nulliparity,
- hyperthyroid,
- obesity,
- decreased in smokers
95
HYPEREMESIS
How is severity assessed?
Pregnancy-Unique Quantification of Emesis (PUQE) –
- <7 mild,
- 7-12 mod,
- >12 severe
96
STAGES OF LABOUR
What is the role of oxytocin in labour?
Produced by hypothalamus, secreted by post. pituitary, surge at labour inhibits progesterone to prepare smooth muscle for uterine contractions, milk ejection reflex postpartum
97
PPH
What is a secondary postpartum haemorrhage (PPH)?
Secondary = excessive blood loss from genital tract between 24h–12w after delivery (can result in Sheehan's syndrome)
98
HELLP
what other condition is HELLP associated with?
- 10% have antiphospholipid syndrome
99
HELLP
what are the risk factors for HELLP?
➢ White ethnicity
➢ Maternal age >35 yrs.
➢ Obesity
➢ Chronic hypertension
➢ DM
➢ Autoimmune disorders
➢ Abnormal placentation and multiple gestation
➢ Previous pregnancy with preeclampsia
100
HELLP
what is the management for HELLP?
➢ Seizure prophylaxis (magnesium sulfate), IV dexamethasone, labetalol. IM beclametasone
when patient <36wks
➢ Delivery is definitive treatment (should be done when patient is 37+ wks)
101
FOETAL HYDROPS
what is the pathophysiology?
an imbalance of interstitial fluid production and inadequate lymphatic return. This can result from congestive heart failure, obstructed lymphatic flow, or decreased plasma osmotic pressure.
102
FOETAL HYDROPS
what are the causes of immune foetal hydrops?
results from blood group incompatibility between the mother and the fetus causing fetal anaemia.
THIS IS RHESUS DISEASE OF THE NEWBORN**
103
FOETAL HYDROPS
what are the causes of non-immune foetal hydrops
- severe anaemia (parvovirus B19, thalassaemia, G6PD)
- cardiac abnormalities
- chromosomal abnormalities (trisomies 13, 18 and 21)
- genetic conditions
- other infections (toxoplasmosis, rubella, CMV, varicella)
- structural abnormalities (CCAM, diaphragmatic hernia)
- twin-to-twin transfusion syndrome
- chorioangioma
104
FOETAL HYDROPS
what is the management?
depends on the cause
- anaemia = in-utero blood transfusion
- pleural effusions/CCAM = shunt
- twin-to-twin transfusion syndrome = laser photocoagulation of placental anastomoses
- cardiac arrhythmias = maternal digoxin + flecanide
105
UTEROPLACENTAL INSUFFICIENCY
what are the causes of uteroplacental insufficiency?
➢Abnormal trophoblast invasion:
▪ Pre-eclampsia
▪ Placenta accreta
➢ Abruption
➢ Infarction
➢ Placenta previa
➢ Tumor: chorioangiomas
➢ Abnormal umbilical cord or cord insertion (i.e., two vessel cord)
➢ Maternal diabetes
➢ Maternal hypertension
➢ Anemia
➢ Smoking
➢ Drug abuse (cocaine, heroin, methamphetamine)
➢ Antiphospholipid syndrome
➢ Renal disease
➢ Advanced age
106
UTEROPLACENTAL INSUFFICIENCY
what is the presentation?
➢ Depending on the cause
➢ Mother may notice uterus is smaller than previous pregnancies
➢ Fetus may be moving less than expected
➢ IUGR
➢ Vaginal bleeding or preterm labor contractions (i.e., during placental abruption)
107
PUERPERAL INFECTION
what is it defined as?
Temperature of above 38 degrees Celsius in the first 14 days following delivery.
108
PUERPERAL INFECTION
what is the management?
➢ Supportive (analgesics/NSAIDS, wound care, ice packs...)
➢ Antibiotics (for endometritis – IV clindamycin and gentamicin until >24hrs afebrile)
➢ Surgical (drain abscess, secondary repair of wound, drainage of hematomas...)
109
OBSTRUCTED LABOUR
What are the different types of causes of obstructed labour?
- Power (most common)
- Passage
- Passenger
- Psyche (maternal exhaustion in second stage)
110
MISCARRIAGE
What is the management of antiphospholipid syndrome?
Low dose aspirin + LMWH
111
CHORIONIC VILLUS SAMPLING
when is chorionic villus sampling performed?
Usually between 10-13 weeks
112
AMNIOCENTESIS
When is amniocentesis performed?
from 15 weeks onwards
113
CHLAMYDIA IN PREGNANCY
what is the management?
- azithromycin 1g OD followed by 500mg orally OD for 2 days
- erythromycin 500mg QD for 7 days
- amoxicillin 500mg TD for 7 days
114
GONORRHOEA IN PREGNANCY
what are the risks?
- miscarriage
- premature birth
- low birth weight
- PROM
- chorioamnionitis
- eye infection in newborn
115
GONORRHOEA IN PREGNANCY?
what is the management?
500mg ceftriaxone IM single dose
116
SYPHILIS IN PREGNANCY
what is the management?
penicillin
117
TRICH VAGINALIS IN PREGNANCY
what is the management?
metronidazole
118
UTIs IN PREGNANCY
what are the treatments?
* Oral antibiotics
- Asymptomatic bacteriuria: 3 days
- Cystitis 7 days
- nitrofurantoin (avoid in 3rd trimester)
- amoxicillin (only once sensitivities known)
- cefalexin
119
UTIs IN PREGNANCY
what is the management of pyelonephritis?
antibiotics (IV) for 10-14 days
- Pyelonephritis needs IV antibiotics until pyrexia settles and vomiting stops. IV fluids and antipyretics too.
120
UTIs IN PREGNANCY
what are the antenatal risk factors for UTIs?
- previous infection
- renal stones
- diabetes mellitus
- immunosuppression
- polycystic kidneys
- congenital abnormalites of renal tract
- neuropathic bladder
121
CEPHALOPELVIC DISPROPORTION
what can increase the risk?
- flat (platypelloid) pelvic opening
- heart-shaped (android) pelvis
122
MISCARRIAGE
what is the management of a threatened miscarriage?
vaginal progesterone 400mg BD
offered to women with confirmed intrauterine pregnancy, if they have vaginal bleeding and previous miscarriage
if foetal heartbeat is confirmed, continue progesterone until 16 weeks
123
ANAEMIA + PREGNANCY
what are the cut offs for the normal ranges of haemoglobin during pregnancy?
1st trimester = <110g/L
2nd/3rd trimester = <105g/L
Postpartum = <100g/L
124
PREMATURE LABOUR
how can premature labour be prevented?
- vaginal progesterone gel/pessary (if cervical length <25mm on vaginal USS at 16-24 weeks)
- cervical cerclage (if cervical length <25mm on vaginal USS at 16-24 weeks and have had previous premature birth or cervical trauma)
- rescue cervical cerclage offered at 16-27+6 weeks when there is cervical dilatation without ROM
125
PREMATURE LABOUR
what medications can stop uterine contractions?
when are they used?
- nifedipine or atosiban
- used between 24-33+6 weeks
- used to delay delivery and buy time for further foetal development, administration of steroids or transfer to a more specialist unit
- only used as a short term measure (<48 hours)
126
FIBROIDS
What are some risk factors for fibroids?
- Afro-Caribbean
- Obesity
- Early menarche
- FHx
- Increasing age (until menopause)
127
FIBROIDS
What is the first line non-hormonal management of fibroids <3cm?
- Tranexamic acid (antifibrinolytic) taken during bleeding to reduce it
- Mefenamic acid (NSAID) to reduce bleeding + pain
128
FIBROIDS
What is the first line hormonal management of fibroids <3cm?
- Mirena coil is 1st line (fibroids <3cm with no uterus distortion)
- 2nd = COCP triphasing (back-to-back for 3m then break)
- Cyclical oral progestogens
- Norethisterone 5mg TDS can be used short-term to rapidly stop menorrhagia from 3d before period until bleeding acceptable
129
FIBROIDS
What is the management of fibroids >3cm?
- Same medical Mx but surgery offered too
- GnRH agonists (goserelin) can be given to shrink fibroids by inducing menopausal state (reduced oestrogen) in short-term (can demineralise bone) for surgery
- Selective progesterone receptor modulators (SPRMS) like ulipristal acetate can be used instead to avoid SEs
130
ADENOMYOSIS
What are the investigations for adenomyosis?
- Bimanual exam = bulky + tender uterus, 'BOGGY'
- TVS is 1st line investigation
- Gold standard - histological examination of uterus after hysterectomy (not always suitable though)
131
ADENOMYOSIS
What is the initial management of adenomyosis?
if pt does NOT want contraception
- anti-fibrinolytic = TRANEXAMIC ACID (when there is no associated pain)
- NSAID = MEFANAMIC ACID (when there is associated pain)
if pt does want contraception
- 1st line = mirena coil
- COCP
- cyclical oral progestogens
other options (considered by specialist)
- GnRH analogues
- endometrial ablation
- uterine artery embolism
- hysterectomy
132
ENDOMETRIOSIS
What are some risk factors for endometriosis?
- Early menarche,
- late menopause,
- obstruction to vaginal outflow (imperforate hymen)
133
ENDOMETRIOSIS
What is the initial management of endometriosis?
- NSAIDs ± paracetamol first line for Sx relief
- COCP triphasing (can't take for longer as if not irregular bleeding
- POP like medroxyprogesterone acetate
- GnRH analogues to "induce" menopause, reversible, quicker than triphasing but need HRT + only short-term as risk of osteoporosis
134
PCOS
How does insulin resistance contribute to PCOS?
- Insulin resistance = pancreas produces more insulin
- Insulin mimics action of insulin-like growth factor 1 which augments androgen production by theca cells in response to LH
- Higher insulin = higher androgens (testosterone)
135
PCOS
How does high insulin levels contribute to PCOS?
- Insulin suppresses sex hormone-binding globulin (SHBG) produced by liver which normally binds to androgens + suppresses their function further promoting hyperandrogenism
- Also contribute to halting development of follicles in ovaries > anovulation + multiple partially developed follicles (polycystic ovaries)
136
PCOS
What are the 3 main presenting features of PCOS?
- Hyperandrogenism
- Insulin resistance
- Oligo or amenorrhoea + sub/infertility
137
PCOS
How does insulin resistance present?
- Obesity, acanthosis nigricans (thickened, rough skin often axilla + elbows with velvety texture), psychological Sx
138
PCOS
What diagnostic criteria is used in PCOS?
Rotterdam criteria (≥2) –
- Oligo- or anovulation (may present as oligo- or amenorrhoea)
- Hyperandrogenism (biochemical or clinical)
- Polycystic ovaries (≥12) or ovarian volume >10cm^3 on USS
139
PCOS
What hormone tests may be used in PCOS?
- Testosterone (raised)
- SHBG (low)
- LH (raised) + raised LH:FSH ratio (LH>FSH)
- Prolactin (normal), TFTs (exclude causes)
140
PCOS
What other investigation may be useful at indicating PCOS?
2h 75g OTT for DM –
- IFG = 6.1–6.9mmol/L
- IGT (at 2h) = 7.8–11.1
- Diabetes (at 2h) = >11.1
141
PCOS
What are some associations and complications of PCOS?
- DM, CVD + hypercholesterolaemia
- Obstructive sleep apnoea, MH issues, sexual problems
- Endometrial hyperplasia or cancer
142
PCOS
What are the PCOS risk factors for endometrial cancer?
How is the risk of endometrial cancer managed in PCOS?
- Obesity, DM, insulin resistance, amenorrhoea
- Mirena coil for continuous endometrial protection
- Induce withdrawal bleed AT LEAST every 3m with COCP or cyclical progesterones medroxyprogesterone 10mg 14d)
143
PCOS
How is infertility managed in PCOS?
- Weight loss initial step to restore regular ovulation
- Clomiphene to induce ovulation
- Metformin may help (+ helps insulin resistance)
- Laparoscopic ovarian drilling or IVF last resort
144
CERVICAL CANCER
What genes may be implicated in cervical cancer?
- P53 + pRb are tumour suppressor genes
- HPV produces two oncoproteins (E6 + E7)
- E6 inhibits P53, E7 inhibits pRB
145
CERVICAL CANCER
How is cervical cancer staged?
FIGO staging –
- 1 = confined to cervix
- 2 = invades uterus or upper 2/3 vagina
- 3 = invades pelvic wall (e.g. ureter) or lower 1/3 vagina
- 4 = invades beyond pelvis
146
CERVICAL CANCER
What is the cervical cancer screening?
- Sexually active women 25–64 (triennially 25–50, 5y 50–64) smear test
- Exceptions = HIV pts screened annually, women with previous CIN may require additional tests
147
CERVICAL CANCER
What is used to grade the level of dysplasia, or premalignant change, in the cells of the cervix after colposcopy?
- Cervical intra-epithelial neoplasia (CIN)
- CIN I = mild, affects 1/3 thickness of epithelial layer, likely to return to normal without Tx
- CIN II = mod, affects 2/3 thickness of epithelial layer, likely to progress to cancer without Tx
- CIN III or cervical carcinoma in situ = severe, v likely to progress to cancer without Tx
148
OVARIAN CANCER
What are the 4 types of ovarian cancer?
- Epithelial cell tumours (85–90%)
- Germ cell tumours (common in women <35)
- Sex cord-stromal tumours (rare)
- Metastatic tumours
149
OVARIAN CANCER
What are some types of epithelial cell tumours?
- Serous carcinoma (#1)
- Endometrioid, clear cell, mucinous + undifferentiated tumours too
150
OVARIAN CANCER
What are sex-cord stromal tumours?
- Arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles)
- Sertoli-Leydig + granulosa cell tumours
151
OVARIAN CANCER
What are metastatic tumours?
- Secondary tumours
- Krukenberg = metastasis in ovary, usually from GI (stomach) > CLASSIC "SIGNET-RING" CELLS ON HISTOLOGY
152
OVARIAN CANCER
What are some risk factors of ovarian cancer?
Unopposed oestrogen + increased # of ovulations –
- Early menarche
- Late menopause
- Increased age
- Endometriosis
- Obesity + smoking
Genetics (BRCA1/2, HNPCC/lynch syndrome)
153
OVARIAN CANCER
Hence, what are some protective factors of ovarian cancer?
- COCP
- Early menopause
- Breast feeding
- Childbearing
154
OVARIAN CANCER
How is the risk of malignancy index calculated?
- Menopausal status = 1 (pre) or 3 (post)
- Pelvic USS findings = 1 (1 feature) or 3 (>1 feature)
- CA-125 levels IU/mL as marker for epithelial cell ovarian cancer
155
OVARIAN CANCER
What can cause falsely elevated CA-125 levels?
- Endometriosis
- Fibroids + adenomyosis
- Pelvic infection
- Pregnancy
- Benign cysts
156
OVARIAN CANCER
What staging is used in ovarian cancer?
FIGO staging –
- 1 = confined to ovary
- 2 = past ovary but contained to pelvis
- 3 = past pelvis but inside abdomen (can be microscopically in lining of abdomen)
- 4 = spread to other organs
157
OVARIAN CYST
What are the 4 types of ovarian cysts?
- Functional (physiological)
- Benign epithelial neoplasms
- Benign germ cell neoplasms
- Benign sex-cord stromal neoplasms
158
OVARIAN CYST
What are the three types of functional cysts?
- Follicular (most common)
- Corpus luteum
- Theca lutein
159
OVARIAN CYST
What are corpus luteum cysts?
When are they seen?
- Corpus luteum fails to breakdown, may fill with fluid or blood
- May burst causing intraperitoneal bleeding
- Early pregnancy
160
OVARIAN CYST
What are theca lutein cysts?
Association?
- Stimulates growth of follicular theca cells so usually bilateral as resting follicles on both sides
- Overstimulation of hCG (multiple + molar pregnancy as hCG v high)
161
OVARIAN CYST
What are some features of neoplastic cysts?
- Often complex
- >10cm
- Irregular borders
- Internal septations appearing multi-locular
- Heterogenous fluid
162
OVARIAN CYST
What are the 2 benign epithelial neoplasms?
- Serous cystadenoma (most common epithelial tumour)
- Mucinous cystadenoma
163
OVARIAN CYST
How does serous cystadenoma present?
- May be bilateral, filled with watery fluid, 30–50y
164
OVARIAN CYST
How does mucinous cystadenoma present?
- Often very large + contain mucus-like fluid
- Pseudomyxoma peritonei where abdo cavity fills with gelatinous mucin secretions if rupture
- 30–40y
165
OVARIAN CYST
What are benign germ cell neoplasms?
- Dermoid cysts or teratomas
- Common in women <35
- May contain various tissue types (skin, teeth, hair + bone)
- Can be bilateral, associated with ovarian torsion as heavy
166
OVARIAN CYST
What is an example of sex cord-stromal neoplasms?
- Fibromas (small, solid benign fibrous tissue tumour)
- Associated with Meig's syndrome
167
OVARIAN CYST
What are some risk factors of ovarian cysts?
- Obesity, tamoxifen, early menarche, infertility
- Dermoid cysts = most common in young women, can run in families
- Epithelial cysts = most common in post-menopausal (?malignant)
168
OVARIAN CYST
What investigations should be done for ovarian cysts?
- Beta-hCG to exclude uterine or ectopic
- FBC for infection or haemorrhage
- CA-125 if >40
- Germ cell tumour markers if <40 with complex ovarian mass
- Imaging (TVS or MRI abdo if larger mass)
- Diagnostic laparoscopy (gold standard in ruptured cyst)
- May need USS guided aspiration + cytology to confirm benign
169
OVARIAN CYST
What are the germ cell tumour markers?
- Lactate dehydrogenase
- Alpha-fetoprotein
- Human chorionic gonadotropin
170
OVARIAN CYST
What is the management of simple cysts in pre-menopausal women?
- Small <5cm = likely to resolve within 3 cycles, no follow up
- Mod 5–7cm = routine gynae referral + yearly USS
- Large >7cm = ?MRI + surgical evaluation
171
OVARIAN CYST
What is the management of post-menopausal women presenting with an ovarian cyst?
- Risk of malignancy index calculation
- Simple cysts <5cm + normal CA-125 = monitor with 4–6m USS
- Complex cyst or raised CA-125 = 2ww gynae oncology referral
172
ENDOMETRIAL CANCER
What are some risk factors for endometrial cancer?
Unopposed oestrogen –
- Obesity (adipose tissue contains aromatase)
- Nulliparous
- Early menarche
- Late menopause
- Oestrogen-only HRT
- Tamoxifen
- PCOS
- Increased age
- T2DM
- HNPCC (Lynch syndrome)
173
ENDOMETRIAL CANCER
What are some protective factors for endometrial cancer?
- COCP
- Mirena coil
- Multiparity
- Cigarette smoking (Seem to have anti-oestrogenic effect)
174
ENDOMETRIAL CANCER
What is the staging for endometrial cancer?
FIGO staging –
- 1 = confined to endometrium + uterus
- 2 = tumour invaded cervix
- 3 = cancer spread to ovary, vagina, fallopian tubes or LN
- 4 = cancer invades bladder, rectum or beyond pelvis
175
ENDOMETRIAL POLYP
What are some risk factors of endometrial polyps?
- Being peri or post-menopausal
- HTN
- Obesity
- Tamoxifen
176
VULVAL CANCER
What is vulval cancer?
What is the most common histological type?
- Rare compared to other cancers
- Squamous cell carcinomas (90%), malignant melanoma less common
177
VULVAL CANCER
What are some risk factors for vulval cancer?
- Vulval intraepithelial neoplasia (VIN) due to HPV in younger women
- Lichen sclerosus in older women
178
VULVAL CANCER
How is vulval cancer staged?
FIGO staging –
- 1 = <2cm
- 2 = >2cm
- 3 = adjuvant organs or unilateral nodes
- 4 = distant mets or bilateral nodes
179
VULVAL CANCER
What is the management of VIN?
- Biopsy to Dx
- Watch + wait with close follow up
- Wide local excision to surgically remove lesion
- Imiquimod cream or laser ablation
180
VAGINAL CANCER
What is the most common histological type of vaginal cancer?
- 90% squamous
181
MENOPAUSE
What are the peri-menopausal symptoms?
- Vasomotor = hot flushes, night sweats, impact on QOL
- General = mood swings, decreased libido, vaginal dryness, headache, dry skin, loss of energy, joint aches, muscles pains, irregular periods
182
MENOPAUSE
Why does urogenital atrophy occur?
- Urogenital tract has oestrogen receptors + continual stimulation keep it strong + supple
183
MENOPAUSE
What contraception is suitable in older women?
How do hormonal contraceptives affect the menopause?
- UKMEC1 = barrier, IUS/IUD, POP, long-acting progesterone (<45), sterilisation
- UKMEC2 = COCP after 40 used until 50, try ones with levonorgestrel or norethisterone as lower VTE risk
- They don't but may mask Sx
184
MENOPAUSE
What is the management of menopause in more severe cases?
- HRT first-line for vaso-motor Sx as most effective
- Clonidine (alpha adrenergic receptor agonist) second line with low-dose antidepressants like venlafaxine (not C/I in breast cancer Tx) or fluoxetine
- CBT
- Vaginal oestrogen cream/tablets + moisturisers for dryness
185
MENOPAUSE
What is the mechanism of action of clonidine?
- Alpha-adrenergic receptor agonist
186
HRT
What are some benefits of HRT?
- Improved Sx control
- Improved QOL
- Reduced risk of osteoporosis
187
HRT
What are some risks with HRT?
- Increased risk of breast cancer by adding progesterone
- Increased risk of endometrial cancer by oestrogen alone
- Increased risk of VTE
- Increased risk of stroke + IHD
188
HRT
What are some contraindications to HRT?
- Undiagnosed PV bleeding
- Current or past breast cancer
- Any oestrogen sensitive cancer (endometrial)
189
HRT
What HRT would you give to...
i) woman without uterus?
ii) woman with uterus?
iii) woman with period within past 12m?
iv) woman with period >12m ago?
i) Continuous oestrogen-only HRT
ii) Add progesterone (combined HRT)
iii) Cyclical combined HRT
iv) Continuous combined HRT
190
HRT
What are the side effects associated with oestrogen?
- Nausea,
- bloating,
- headaches,
- breast swelling or tenderness,
- leg cramps
191
ATROPHIC VAGINITIS
What is the pathophysiology of atrophic vaginitis?
- Epithelial lining of vagina + urinary tract responds to oestrogen by becoming thicker, more elastic + producing secretions so reduced oestrogen has opposite effect
- Tissue more prone to inflammation + changes in vaginal pH + microbial flora that contribute to localised infections
192
ATROPHIC VAGINITIS
What are some risk factors for atrophic vaginitis?
- Menopause
- Oophorectomy
- Anti-oestrogen (tamoxifen, anastrozole)
193
URINARY INCONTINENCE
What is the physiology of micturition?
- Detrusor = smooth muscle, transitional epithelium normally only contracts during micturition = sacral parasympathetic innervation from S2-4
- M2+3 muscarinic receptors with ACh
- Sympathetic nerve fibres from T11-L2 maintain relaxation of bladder for storage
194
URINARY INCONTINENCE
What causes urge incontinence/OAB?
- Overactivity + involuntary contractions of the detrusor muscle
195
URINARY INCONTINENCE
What are some causes of overflow incontinence?
- Anticholinergics
- Fibroids
- Pelvic tumours
- BPH (men)
- Neuro (damage, MS, diabetic neuropathy, spinal cord injuries)
196
URINARY INCONTINENCE
What is the stepwise management of urge incontinence/OAB?
- 1st line = bladder retraining (6w gradually increasing time between voiding)
- 1st line drugs = anti-muscarinics (oxybutynin, tolterodine, darifenacin)
- Mirabegron (beta-3-adrenergic agonist) if anti-muscarinics not tolerated
- specialist referral for botox injections + surgery
197
URINARY INCONTINENCE
What is the mechanism of action of anti-muscarinics?
- Parasympathetic so Pissing = decreases need to urinate + spasms
198
URINARY INCONTINENCE
What is the mechanism of action of beta-3-adrenergic agonists?
- Sympathetic so Storage = relaxes detrusor + increases bladder capacity
199
URINARY INCONTINENCE
What are last resort options for urge incontinence?
- Augmentation cystoplasty with bowel tissue
- Bypass (urostomy)
- Botox can paralyse detrusor + block ACh release
200
URINARY INCONTINENCE
What are the surgical interventions for stress incontinence?
- Colposuspension
- Tension free vaginal tape (TVT)
- Autologous sling procedures (TVT but strip of fascia from abdo wall)
201
PELVIC ORGAN PROLAPSE
What are some risk factors of pelvic organ prolapse?
- Age
- BMI
- Multiparity (vaginal)
- Spina bifida
- Pelvic surgery
- Menopause
202
PELVIC ORGAN PROLAPSE
What are the investigations for pelvic organ prolapse?
- Sim's speculum (U-shaped) to show if something is there
- May have urodynamics, USS or MRI
203
PELVIC ORGAN PROLAPSE
What is the management for pelvic organ prolapse?
- Conservative = pelvic floor exercises, weight loss + diet changes
- Vaginal pessary = ring (preferred as can have sex), shelf or Gellhorn
- Surgery (symptomatic or severe like outside vagina, ulcerated, failed Mx)
204
DYSMENORRHOEA
What is the management of primary dysmenorrhoea?
- NSAIDs like mefenamic acid during menstruation
- COCP second line
205
ASHERMAN'S SYNDROME
What causes Asherman's syndrome?
- Pregnancy-related dilatation + curettage procedures
- After uterine surgery
- Pelvic infection like endometritis
206
ASHERMAN'S SYNDROME
What is the clinical presentation of Asherman's syndrome?
- Secondary amenorrhoea
- Infertility
- Significantly lighter periods
- Dysmenorrhoea
207
ASHERMAN'S SYNDROME
What is the management of Asherman's syndrome?
- Hysterosalpingography = contrast injected into uterus + XR
- Sonohysterography = uterus filled with fluid + pelvic USS
- Hysteroscopy gold standard + can dissect adhesions (recurrence after common)
208
ENDOMETRIOSIS
What are some protective factors?
Multiparity + COCP
209
CERVICAL CANCER
What is cervical cancer?
What is the histological type of cervical cancer?
- Most common cancer in women <35
- Squamous cell carcinoma 80%, then adenocarcinoma (small cell rare)
210
VAGINAL CANCER
What causes it?
HPV or metastatic spread from cervix or vulva
211
HRT
What are the side effects associated with progesterone?
Mood swings,
fluid retention,
weight gain,
acne
greasy skin
212
HYDATIDIFORM MOLE
What is a complete mole?
- Diploid trophoblast cells
- Empty egg + sperm that duplicates DNA (all genetic material comes from father)
- 46 chromosomes
- No foetal tissue
213
HYDATIDIFORM MOLE
What is a partial mole?
- Triploid (69XXX, 69XXY) trophoblast cells
- 2 sperm fertilise 1 egg
- Some recognisable foetal tissue
214
HYDATIDIFORM MOLE
What is an invasive mole?
What is the significance of this?
- When a complete mole invades the myometrium
- Metaplastic potential to evolve into a choriocarcinoma
215
HYDATIDIFORM MOLE
What are some risk factors for hydatidiform mole?
- Extremes of reproductive age
- Previous molar pregnancy
- Multiple pregnancies
- Asian women
- OCP
216
PELVIC INFLAMMATORY DISEASE
What are the STI causes of PID?
- N. gonorrhoea (tends to be more severe),
- chlamydia trachomatis (most common),
- Mycoplasma genitalium
217
PID
What might you look for on microscopy in PID?
What is the relevance?
- Pus cells on swabs from vagina or endocervix
- Absence is useful to exclude PID
218
PELVIC INFLAMMATORY DISEASE
What is the management of PID?
- 1g stat IM ceftriaxone (gonorrhoea)
- 100mg BD doxycycline for 14d (chlamydia + MG)
- Metronidazole 400mg BD for 14d (Gardnerella)
- GUM referral for specialist Mx + contact tracing
- Hospital admission for IV Abx if signs of sepsis or pregnant
- Pelvic abscess > drainage
219
PELVIC INFLAMMATORY DISEASE
What are the non-infective causes of PID?
- Post-partum (retained tissue),
- uterine instrumentation (hysteroscopy, IUCD),
- descended from other organs (appendicitis)
220
PELVIC INFLAMMATORY DISEASE
What are the non-STI infective causes of PID?
Gardnerella vaginalis,
H. influenzae,
E. coli.
221
GENITAL TRACT FISTULA
what are the causes of genital tract fistulas?
injury (primarily in childbirth),
surgery,
infection
radiation.
222
CERVICAL CANCER SCREENING
when is screening offered?
25-49yrs = every 3 years
50-64yrs = every 5 years
not offered to people over 64yrs
223
URINARY INCONTINENCE
What are some side effects of anti-muscarinics?
- "Can't see, spit, pee or shit" > caution in elderly as falls esp oxybutynin immediate release in frail
224
URINARY INCONTINENCE
What is a caution of beta-3-adrenergic agonists?
- C/I in uncontrolled HTN as stimulates SNS to increase BP, can lead to hypertensive crisis so monitor BP
225
DYSMENORRHOEA
What is secondary dysmenorrhoea?
Secondary to endometriosis, adenomyosis, fibroids, PID, IUDs, cancer
