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C TO REVISE - PHASE 3A > WOMENS HEALTH - OBSTETRICS AND GYNAE > Flashcards

WOMENS HEALTH - OBSTETRICS AND GYNAE Flashcards

1
Q

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

A
  • PV/PO synthetic prostaglandin misoprostol
  • Contact HCP if no bleeding in 24h
  • Urinary beta-hCG 3w after to exclude ectopic or molar
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2
Q

HYPEREMESIS
What is the diagnostic triad for hyperemesis gravidarum?

A

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

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3
Q

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

A

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

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4
Q

PLACENTA PRAEVIA
What are some risk factors for placenta praevia?

A
  • Embryos more likely to implant on lower segment scar from previous c-section
  • Multiple pregnancy
  • Multiparity
  • Previous praevia
  • Assisted conception
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5
Q

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

A
  • IUGR, pre-eclampsia or pre-existing HTN, maternal smoking + previous abruption
  • Cocaine use, multiple pregnancy or high parity, trauma
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6
Q

VASA PRAEVIA
What are some risk factors for vasa praevia?

A
  • Placenta praevia
  • Multiple pregnancy
  • IVF pregnancy
  • Bilobed placentas
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7
Q

PRE-ECLAMPSIA
How can pre-eclampsia be classified?

A
  • Mild-mod = pre-eclampsia without severe HTN (<160/110) and NO Sx, biochemical or haematological impairment
  • Severe = pre-eclampsia w/ severe HTN ± Sx ± biochem ± haem impairment
  • Early <34w, late >34w
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8
Q

PRE-ECLAMPSIA
What is the result of placental ischaemia?

A
  • Pro-inflammatory protein + thromboplastin release leads to endothelial damage > vasoconstriction, clotting dysfunction + increased vascular permeability
  • Ultimately leads to poor renal perfusion > RAAS activation > HTN, proteinuria ± oedema > pre-eclampsia + eclampsia (if continues)
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9
Q

PRE-ECLAMPSIA

What are the…

i) high risk
ii) moderate risk

factors for pre-eclampsia?

A

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

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10
Q

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

A
  • Local areas of vasospasm leading to hypoperfusion
  • Oedema due to increased vascular permeability + hypoproteinaemia
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11
Q

PRE-ECLAMPSIA
What blood investigations would you do in pre-eclampsia?

A
  • FBC with platelets (thrombocytopenia)
  • Serum uric acid levels (raised due to renal issues)
  • LFTs (elevated liver enzymes ALT + AST)
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12
Q

PRE-ECLAMPSIA
What other investigations could you perform in pre-eclampsia?

A
  • Proteinuria on dipstick (++ or +++ is severe)
  • Protein:Creatinine ratio (PCR) ≥30ng/nmol = significant proteinuria
  • Accurate dating + USS to assess foetal growth
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13
Q

IUGR
What are the 3 broad categories causing IUGR?

A
  • Placental insufficiency (most common cause)
  • Maternal factors
  • Foetal factors
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14
Q

IUGR
What are some maternal causes of IUGR?

A
  • Chronic disease (HTN, cardiac, CKD)
  • Substance abuse (cocaine, alcohol) smoking, previous SGA baby
  • Autoimmune
  • Low socioeconomic status
  • > 40
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15
Q

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

A
  • SFH < 10th centile, slow or static growth or crossing centiles
  • Refer for serial growth scans (USS) every 2w, umbilical artery doppler + amniotic fluid volume
  • MCA doppler performed after 32w
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16
Q

MULTIPLE PREGNANCY
What are some predisposing factors to multiple pregnancies?

A
  • Previous twins,
    FHx,
    increasing parity + maternal age,
    IVF,
    race (Afro-Caribbean)
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17
Q

MULTIPLE PREGNANCY
What is the management of multiple pregnancies?

A
  • Steroids if <34w
  • Monochorionic/amniotic twins = elective c-section 32-34w
  • Diamniotic twins = 37–38w, vaginal if presenting twin cephalic but may need c-section for second
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18
Q

OLIGOHYDRAMNIOS
What are some causes of oligohydramnios?

A
  • PROM or SROM
  • Renal agenesis (Potter’s syndrome) or non-functional kidneys
  • Placental insufficiency (pre-eclampsia, post-term gestation) as blood redistributed to brain so reduced urine output
  • Genetic anomalies
  • Obstructive uropathy
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19
Q

POLYHYDRAMNIOS
What are the causes of polyhydramnios?

A
  • Increased foetal urine production (maternal DM), twin-twin transfusion, foetal hydrops
  • Foetal inability to swallow/absorb amniotic fluid (GI tract obstruction e.g. duodenal atresia, foetal neuro/muscular issues)
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20
Q

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

A
  • Rh-ve woman exposed to Rh+ve foetal blood, her immune system recognises as foreign + produce antibodies against rhesus D (sensitisation)
  • Usually no issues in 1st pregnancy as IgM produced that cannot cross placenta
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21
Q

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

A
  • Memory cells produce IgG which can cross placenta so if Rh+ve foetus will attack leading to haemolysis (haemolytic disease of newborn) with jaundice + hydrops fetalis (abnormal accumulation of fluid)
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22
Q

GESTATIONAL DIABETES
What are some anti-insulin hormones produced by the placenta?

A
  • Main one is human placental lactogen (hPL)
  • Also glucagon + cortisol
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23
Q

INFECTIONS + PREGNANCY
What are the risks of Varicella zoster?

A
  • Maternal risk = 5x greater risk of pneumonitis
  • Foetal varicella syndrome = skin scarring, microphthalmia, limb hypoplasia, microcephaly + learning difficulties
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24
Q

PROM
What is the management of PPROM?

A
  • 1st line = IM corticosteroids if foetus <34w
  • Prophylactic PO erythromycin given to prevent chorioamnionitis for 10d or until labour is established if within 10d
  • Consider induction at 34w (trade off)
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25
Q

STAGES OF LABOUR
What are 7 important hormones in labour?

A
  • Prostaglandins
  • Oxytocin
  • Oestrogen
  • Beta-endorphins
  • Adrenaline
  • Prolactin
  • Relaxin
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26
Q

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

A
  • Occiput transverse
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27
Q

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

A
  • Idiopathic
  • Prematurity as baby may not have turned itself yet
  • Previous breech
  • Uterine abnormalities (bicornuate uterus), fibroids
  • Placenta praevia
  • Foetal abnormalities (CNS malformation
  • Multiple pregnancy
  • Poly/oligohydramnios
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28
Q

BREECH
What are some contraindications for ECV?

A
  • Absolute = pre-eclampsia, APH, oligohydramnios, foetal compromise
  • Relative = maternal HTN, foetal abnormality, 1 previous c-section
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29
Q

CTG
What does reduced variability tell you?

A
  • Reduced variability may be hypoxia, lactic acidosis, prematurity
  • 40m reduced variability accepted as baby may be sleeping
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30
Q

SHOULDER DYSTOCIA
Explain what is the result of…

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

A

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

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31
Q

SHOULDER DYSTOCIA
What are the 3 rotational manoeuvres?

A
  • Rubin II = pressure on post. aspect of ant. shoulder to help deliver under symphysis pubis
  • Woods’ screw = Rubin II + pressure on ant. aspect of post. shoulder
  • Reverse woods’ screw = pressure on ant. aspect of ant. shoulder + post. aspect of post. shoulder in opposite way
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32
Q

C-SECTION
What are the complications of c-sections?

A
  • Surgical risk (bleeding, infection/endometritis, VTE)
  • Damage risk (ureter, bladder, bowel, vessels)
  • Future pregnancies (increased risk of uterine rupture, placenta praevia, stillbirth + repeat section)
  • Baby (risk of lacerations, increased incidence in transient tachypnoea)
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33
Q

PAIN RELIEF
What causes labour pain in…

i) first stage?
ii) second stage?

A

i) Uterine contraction at T10-L1
ii) Perineum + vaginal stretching S2-4 (pudendal)

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34
Q

PAIN RELIEF
What are some complications of regional techniques?

A
  • Potential for spinal cord damage
  • Hypotension + bradycardia
  • Haematoma/abscess at injection site
  • Anaphylaxis if allergic
  • Post-dural puncture headache
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35
Q

UTERINE RUPTURE
What are some risk factors for uterine rupture?

A
  • VBAC
  • Previous uterine surgery
  • Increased BMI
  • High parity
  • Congenital uterine abnormalities
  • Oxytocin use
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36
Q

PPH
What are the primary causes of PPH?

A

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

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37
Q

PPH
What are the risk factors for PPH?

A
  • Before birth = previous PPH, APH, twins/triplets, pre-eclampsia, obesity, polyhydramnios
  • Labour = prolonged, c-section, perineal tear or episiotomy, macrosomia
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38
Q

MENTAL HEALTH
Why can mental health disorders be difficult to detect in the puerperium?

A
  • Fear of treatment
  • Fear of children being removed
  • Cultural lack of recognition
  • Denial
  • Stigma
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39
Q

HYPEREMESIS
What are some associations of hyperemesis gravidarum?

A
  • nulliparity,
  • hyperthyroid,
  • obesity,
  • decreased in smokers
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40
Q

ANAEMIA + PREGNANCY
What are some risk factors?

A

Menorrhagia,
malaria,
hookworm,
twins,
poor diet

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41
Q

HELLP
what are the risk factors for HELLP?

A

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

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42
Q

HELLP
what is the management for HELLP?

A

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

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43
Q

SICKLE CELL DISEASE IN PREGNANCY
what is the management?

A
  • Pre-Pregnancy counselling
  • Stop iron chelating agents before pregnancy
  • Give folic acid and penicillin prophylaxis for hypersplenism
  • Screen for UTI infections each visit
  • Crisis Treatment: Analgesics, oxygen, hydration, and
    antibiotics if infection is suspected
  • Regular foetal monitoring
  • Aim for vaginal delivery
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44
Q

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

A
  • severe anaemia (parvovirus B19, thalassaemia, G6PD)
  • cardiac abnormalities
  • chromosomal abnormalities (trisomies 13, 18 and 21)
  • genetic conditions
  • other infections (toxoplasmosis, rubella, CMV, varicella)
  • structural abnormalities (CCAM, diaphragmatic hernia)
  • twin-to-twin transfusion syndrome
  • chorioangioma
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45
Q

FOETAL HYDROPS
what is the management?

A

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

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46
Q

LOW BIRTH WEIGHT
what are the causes of low birth weight?

A

➢ Preterm birth (before 37 weeks gestation)
➢ Genetics (could be chromosomal abnormalities…)
➢ Uteroplacental insufficiency
➢ Multiple pregnancy
➢ Substance abuse (smoking, drinking alcohol, illicit drug) causing IUGR
➢ Chronic conditions and infections (hypertension, rubella, CMV, syphilis, toxoplasmosis, BV…)
➢ Medications (sodium valproate, ramipril, warfarin…)

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47
Q

UTEROPLACENTAL INSUFFICIENCY
what are the causes of uteroplacental insufficiency?

A

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

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48
Q

UTEROPLACENTAL INSUFFICIENCY
what are the investigations?

A

➢ USS
➢ Maternal alpha fetoprotein levels
➢ CTG

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49
Q

PUERPERAL INFECTION
what is the management?

A

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

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50
Q

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

A
  • Power (most common)
  • Passage
  • Passenger
  • Psyche (maternal exhaustion in second stage)
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51
Q

CHORIONIC VILLUS SAMPLING
when is chorionic villus sampling performed?

A

Usually between 10-13 weeks

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52
Q

AMNIOCENTESIS
When is amniocentesis performed?

A

from 15 weeks onwards

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53
Q

CHLAMYDIA IN PREGNANCY
what is the management?

A
  • azithromycin 1g OD followed by 500mg orally OD for 2 days
  • erythromycin 500mg QD for 7 days
  • amoxicillin 500mg TD for 7 days
54
Q

UTIs IN PREGNANCY
why are UTIs more common in pregnancy?

A

due to dilation of the upper renal tract and urinary stasis (hypoactive bladder)

55
Q

UTIs IN PREGNANCY
what is the management of pyelonephritis?

A

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

56
Q

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

A
  • previous infection
  • renal stones
  • diabetes mellitus
  • immunosuppression
  • polycystic kidneys
  • congenital abnormalites of renal tract
  • neuropathic bladder
57
Q

UTIs IN PREGNANCY
what is the management?

A

antibiotics (depends on sensitivities)
- penicillin amoxicillin
- cephalosporin
- gentamycin (have to monitor levels to minimise risk of ototoxicity)

58
Q

UTIs IN PREGNANCY
which antibiotics should be avoided in the third trimester and why?

A
  • nitrofurantoin - risk of haemolytic anaemia in newborn with G6PD
  • sulfonamides - risk of kernicterus in newborn due to displacement of protein binding of bilirubin
59
Q

UTIs IN PREGNANCY
which antibiotics are contraindicated in pregnancy?

A
  • tetracyclines - cause permanent staining of teeth and problems with skeletal development
  • ciprofloxacin - causes skeletal problems
60
Q

FIBROIDS
What are the different types of fibroids?

A
  • Intramural (most common) = within the myometrium
  • Subserosal = >50% fibroid mass extends outside uterine contours
  • Submucosal = >50% projection into the endometrial cavity
  • Subserosal + submucosal can be pedunculated (on stalk = risk of torsion)
61
Q

FIBROIDS
What are some risk factors for fibroids?

A
  • Afro-Caribbean
  • Obesity
  • Early menarche
  • FHx
  • Increasing age (until menopause)
62
Q

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

A
  • Tranexamic acid (antifibrinolytic) taken during bleeding to reduce it
  • Mefenamic acid (NSAID) to reduce bleeding + pain
63
Q

ENDOMETRIOSIS
What are 3 theories about the cause of endometriosis?

A
  • Sampson’s = retrograde menstruation (endometrial lining flows backwards through fallopian tubes + into pelvis/peritoneum where endometrial tissue seeds itself
  • Meyer’s = metaplasia of mesothelial cells
  • Halban’s = via blood or lymphatics
64
Q

ENDOMETRIOSIS
What are some risk factors for endometriosis?

A
  • Early menarche,
  • late menopause,
  • obstruction to vaginal outflow (imperforate hymen)
65
Q

PCOS
How does insulin resistance contribute to PCOS?

A
  • Insulin resistance = pancreas produces more insulin
  • Insulin mimics action of insulin-like growth factor 1 which augments androgen production by theca cells in response to LH
  • Higher insulin = higher androgens (testosterone)
66
Q

PCOS
How does high insulin levels contribute to PCOS?

A
  • Insulin suppresses sex hormone-binding globulin (SHBG) produced by liver which normally binds to androgens + suppresses their function further promoting hyperandrogenism
  • Also contribute to halting development of follicles in ovaries > anovulation + multiple partially developed follicles (polycystic ovaries)
67
Q

PCOS
What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism
  • Insulin resistance
  • Oligo or amenorrhoea + sub/infertility
68
Q

PCOS
What are some differentials of hirustism?

A
  • Ovarian or adrenal tumours that secrete androgens
  • Cushing’s syndrome
  • CAH
  • Iatrogenic (steroids, phenytoin)
69
Q

PCOS
How does insulin resistance present?

A
  • Obesity, acanthosis nigricans (thickened, rough skin often axilla + elbows with velvety texture), psychological Sx
70
Q

PCOS
What diagnostic criteria is used in PCOS?

A

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

71
Q

PCOS
What hormone tests may be used in PCOS?

A
  • Testosterone (raised)
  • SHBG (low)
  • LH (raised) + raised LH:FSH ratio (LH>FSH)
  • Prolactin (normal), TFTs (exclude causes)
72
Q

PCOS
What is the gold standard for visualising the ovaries?
What might it show?

A
  • TVS
  • “String of pearls” appearance where follicles arranged around periphery of ovary (≥12 cysts or >10cm^3 ovarian volume)
  • Can also visualise endometrial thickness
73
Q

PCOS
What are some associations and complications of PCOS?

A
  • DM, CVD + hypercholesterolaemia
  • Obstructive sleep apnoea, MH issues, sexual problems
  • Endometrial hyperplasia or cancer
74
Q

PCOS
Why does PCOS increase risk of endometrial hyperplasia + cancer?

A
  • Oligo/anovulation means endometrial lining continues proliferating with unopposed oestrogen as no corpus luteum releasing progesterone
75
Q

PCOS
How is the risks of obesity, T2DM, CVD etc. managed in PCOS?

A
  • Lifestyle > diet + exercise, weight loss to reduce insulin resistance, smoking cessation
  • Orlistat (lipase inhibitor that stops fat absorption in intestines) may be given to assist weight loss if BMI >30kg/^m2
76
Q

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

A
  • Obesity, DM, insulin resistance, amenorrhoea
  • Mirena coil for continuous endometrial protection
  • Induce withdrawal bleed AT LEAST every 3m with COCP or cyclical progesterones medroxyprogesterone 10mg 14d)
77
Q

PCOS
How is hirsutism + acne managed?

A
  • Hair removal cream, topical eflornithine to treat facial hirsutism
  • Co-cyprindiol is COCP licensed for hirsutism + acne as anti-androgen effect but only used for 3m as increased VTE risk
  • Spironolactone by specialist (mineralocorticoid antagonist with anti-androgen effects)
78
Q

CERVICAL CANCER
What has a strong association with development of cervical cancer?

A
  • Human papillomavirus (HPV) types 16 + 18 primarily a STI
  • Also associated with anal, vulval, vaginal, penis, mouth + throat cancers
79
Q

CERVICAL CANCER
How would you confirm a diagnosis of cervical cancer?

A

Colposcopy –
- Acetic acid causes abnormal cells to appear white “acetowhite”
- Schiller’s iodine test = healthy cells stain brown, abnormal do not stain
- Punch biopsy or large loop excision of transformation zone (LLETZ) for histology

80
Q

OVARIAN CANCER
What are the 4 types of ovarian cancer?

A
  • Epithelial cell tumours (85–90%)
  • Germ cell tumours (common in women <35)
  • Sex cord-stromal tumours (rare)
  • Metastatic tumours
81
Q

OVARIAN CANCER
What are some risk factors of ovarian cancer?

A

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

82
Q

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

A
  • COCP
  • Early menopause
  • Breast feeding
  • Childbearing
83
Q

OVARIAN CANCER
What warrants a 2ww gynae oncology referral?

A
  • Ascites
  • Abdo or pelvic mass (unless clearly fibroids)
  • ≥250 risk of malignancy index score
84
Q

OVARIAN CANCER
How is the risk of malignancy index calculated?

A
  • Menopausal status = 1 (pre) or 3 (post)
  • Pelvic USS findings = 1 (1 feature) or 3 (>1 feature)
  • CA-125 levels IU/mL as marker for epithelial cell ovarian cancer
85
Q

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

A
  • Endometriosis
  • Fibroids + adenomyosis
  • Pelvic infection
  • Pregnancy
  • Benign cysts
86
Q

OVARIAN CYST
What are some risk factors of ovarian cysts?

A
  • Obesity, tamoxifen, early menarche, infertility
  • Dermoid cysts = most common in young women, can run in families
  • Epithelial cysts = most common in post-menopausal (?malignant)
87
Q

OVARIAN CYST
What is Meig’s syndrome?
Who is it commonly seen in?
What is the management?

A
  • Triad of fibroma, pleural effusion + ascites
  • Older women
  • Removal of fibroma = complete solution
88
Q

OVARIAN CYST
What are the germ cell tumour markers?

A
  • Lactate dehydrogenase
  • Alpha-fetoprotein
  • Human chorionic gonadotropin
89
Q

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

A
  • Small <5cm = likely to resolve within 3 cycles, no follow up
  • Mod 5–7cm = routine gynae referral + yearly USS
  • Large >7cm = ?MRI + surgical evaluation
90
Q

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

A
  • Risk of malignancy index calculation
  • Simple cysts <5cm + normal CA-125 = monitor with 4–6m USS
  • Complex cyst or raised CA-125 = 2ww gynae oncology referral
91
Q

ENDOMETRIAL CANCER
What is the most common histological type of endometrial cancer?
What are some others?

A
  • Adenocarcinoma (80%)
  • Adenosquamous, squamous, papillary serous, clear cell + uterine sarcoma
92
Q

ENDOMETRIAL CANCER
What are some risk factors for endometrial cancer?

A

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

93
Q

ENDOMETRIAL CANCER
What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking (Seem to have anti-oestrogenic effect)
94
Q

ENDOMETRIAL CANCER
What other investigations is recommended in endometrial cancer?

A
  • Pipelle biopsy via speculum (highly sensitive so useful for exclusion in low risk)
  • Hysteroscopy with endometrial biopsy
  • 2WW urgent gynae oncology referral if PMB in ≥55y
95
Q

ENDOMETRIAL POLYP
What are some risk factors of endometrial polyps?

A
  • Being peri or post-menopausal
  • HTN
  • Obesity
  • Tamoxifen
96
Q

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

A
  • Rare compared to other cancers
  • Squamous cell carcinomas (90%), malignant melanoma less common
97
Q

VULVAL CANCER
What are some risk factors for vulval cancer?

A
  • Vulval intraepithelial neoplasia (VIN) due to HPV in younger women
  • Lichen sclerosus in older women
98
Q

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

A
  • 90% squamous
99
Q

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

A
  • HRT first-line for vaso-motor Sx as most effective
  • Clonidine (alpha adrenergic receptor agonist) second line with low-dose antidepressants like venlafaxine (not C/I in breast cancer Tx) or fluoxetine
  • CBT
  • Vaginal oestrogen cream/tablets + moisturisers for dryness
100
Q

MENOPAUSE
What is the mechanism of action of clonidine?

A
  • Alpha-adrenergic receptor agonist
101
Q

HRT
What are some contraindications to HRT?

A
  • Undiagnosed PV bleeding
  • Current or past breast cancer
  • Any oestrogen sensitive cancer (endometrial)
102
Q

HRT
What are the side effects associated with oestrogen?

A
  • Nausea,
  • bloating,
  • headaches,
  • breast swelling or tenderness,
  • leg cramps
103
Q

ATROPHIC VAGINITIS
What are some risk factors for atrophic vaginitis?

A
  • Menopause
  • Oophorectomy
  • Anti-oestrogen (tamoxifen, anastrozole)
104
Q

URINARY INCONTINENCE
What is the physiology of micturition?

A
  • Detrusor = smooth muscle, transitional epithelium normally only contracts during micturition = sacral parasympathetic innervation from S2-4
  • M2+3 muscarinic receptors with ACh
  • Sympathetic nerve fibres from T11-L2 maintain relaxation of bladder for storage
105
Q

URINARY INCONTINENCE
What are the 6 main types of incontinence?

A
  • Overactive bladder/urge incontinence
  • Stress incontinence
  • Mixed incontinence (of the 2 above)
  • Overflow incontinence
  • Fistula
  • Neurological
106
Q

URINARY INCONTINENCE
What are some risk factors for urinary incontinence?

A
  • Increasing age
  • Multiparity
  • High BMI
  • FHx
  • Previous pelvic surgery (hysterectomy)
107
Q

URINARY INCONTINENCE
What are some investigations in urinary incontinence?

A
  • Hx most important
  • Bladder diary (frequency volume chart) first line
  • Urine dipstick + MSU
  • Residual urine measurement
  • Electronic Personal Assessment Questionnaire
  • Urodynamics
  • Cystogram with contrast
108
Q

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

A
  • Parasympathetic so Pissing = decreases need to urinate + spasms
109
Q

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

A
  • Sympathetic so Storage = relaxes detrusor + increases bladder capacity
110
Q

URINARY INCONTINENCE
What are last resort options for urge incontinence?

A
  • Augmentation cystoplasty with bowel tissue
  • Bypass (urostomy)
  • Botox can paralyse detrusor + block ACh release
111
Q

URINARY INCONTINENCE
What are the surgical interventions for stress incontinence?

A
  • Colposuspension
  • Tension free vaginal tape (TVT)
  • Autologous sling procedures (TVT but strip of fascia from abdo wall)
112
Q

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

A
  • Age
  • BMI
  • Multiparity (vaginal)
  • Spina bifida
  • Pelvic surgery
  • Menopause
113
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for cystocele/cystourethrocele?

A

Anterior colporrhaphy or colposuspension

114
Q

ASHERMAN’S SYNDROME
What is the pathophysiology of Asherman’s?

A
  • Damage to basal layer of endometrium, damaged tissue may heal abnormally, creating scar tissue (adhesions)
  • Adhesions can bind uterine walls together or endocervix, sealing it shut causing obstruction > infertility, 2* amenorrhoea
115
Q

ASHERMAN’S SYNDROME
What causes Asherman’s syndrome?

A
  • Pregnancy-related dilatation + curettage procedures
  • After uterine surgery
  • Pelvic infection like endometritis
116
Q

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

A
  • Secondary amenorrhoea
  • Infertility
  • Significantly lighter periods
  • Dysmenorrhoea
117
Q

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

A
  • Most common cancer in women <35
  • Squamous cell carcinoma 80%, then adenocarcinoma (small cell rare)
118
Q

MENOPAUSE
What can urogenital atrophy lead to?

A

Urinary incontinence + pelvic organ prolapse

119
Q

HRT
What are the side effects associated with progesterone?

A

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

120
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for uterine prolapse?

A

Hysterectomy or sacrohysteropexy

121
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for rectocele?

A

Posterior colporrhaphy

122
Q

HYDATIDIFORM MOLE
What are some risk factors for hydatidiform mole?

A
  • Extremes of reproductive age
  • Previous molar pregnancy
  • Multiple pregnancies
  • Asian women
  • OCP
123
Q

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

A
  • Post-partum (retained tissue),
  • uterine instrumentation (hysteroscopy, IUCD),
  • descended from other organs (appendicitis)
124
Q

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

A

Gardnerella vaginalis,
H. influenzae,
E. coli.

125
Q

GENITAL TRACT FISTULA
what are the different types?

A

➢ Vesicovaginal fistula
➢ Ureterovaginal fistula
➢ Urethrovaginal fistula
➢ Rectovaginal fistula
➢ Enterovaginal fistula
➢ Colovaginal fistula

126
Q

GENITAL TRACT FISTULAS
what are the investigations for genital tract fistulas?

A

➢ Vaginal/anal examination (could use proctoscope or
speculum)
➢ Contrast tests (barium enema)
➢ Blue dye test ➔ put a tampon in the vagina then blue
dye in rectum. If tampon is stained = test positive
➢ CT, MRI, Ultrasound, Manometry

127
Q

OVERACTIVE BLADDER
what are the risk factors for overactive bladder?

A

➢ Old age
➢ Pregnancy/childbirth
➢ Hysterectomy
➢ Obesity
➢ Family history

128
Q

URINARY INCONTINENCE
what can cause stress incontinence?

A
  • low oestrogen in menopause
  • weakened pelvic floor
  • parity
  • pelvic surgery
129
Q

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

A
  • “Can’t see, spit, pee or shit” > caution in elderly as falls esp oxybutynin immediate release in frail
130
Q

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

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

C TO REVISE - PHASE 3A (11 decks)

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