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B TO REVISE - PHASE 3A > B WOMENS TO DO > Flashcards

B WOMENS TO DO Flashcards

1
Q

MISCARRIAGE
What are some other causes of miscarriage?

A
  • PCOS
  • TORCH infections
  • Iatrogenic (amniocentesis, CVS)
  • Smoking, substance abuse
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2
Q

MISCARRIAGE
What are some causes of recurrent miscarriage?

A
  • Antiphospholipid syndrome
  • Hereditary thrombophilias (Factor V leiden deficiency, factor II prothrombin gene mutation, protein C/S deficiency)
  • Uterine abnormalities (uterine septate, fibroids)
  • Poor controlled chronic conditions (DM, thyroid, SLE)
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3
Q

MISCARRIAGE
What are the investigations for recurrent miscarriage?

A

≥3 1st trimester, ≥1 in 2nd –
- Lupus anticoagulant, anti-cardiolipin + phospholipid antibodies
- Thrombophilia screen
- Pelvic USS for structural issues
- Cytogenic analysis of POC after 3rd miscarriage
- Parental blood for karyotyping

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4
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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5
Q

VASA PRAEVIA
What are some risk factors for vasa praevia?

A
  • Placenta praevia
  • Multiple pregnancy
  • IVF pregnancy
  • Bilobed placentas
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6
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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7
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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8
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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9
Q

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

A

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

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10
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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11
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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12
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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13
Q

IUGR
What are the investigations for IUGR?

A
  • BP + urine dipstick (?pre-eclampsia)
  • Karyotyping (?foetal)
  • Infection screen, TORCH (?infection)
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14
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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15
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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16
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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17
Q

OBSTETRIC CHOLESTASIS
Why can clotting be deranged in obstetric cholestasis?

A
  • Bile acids important for fat soluble vitamin absorption like vitamin K
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18
Q

OBSTETRIC CHOLESTASIS
What are the complications of obstetric cholestasis?

A
  • Maternal = vitamin K deficiency (may lead to PPH)
  • Foetal = stillbirth (#1), increased risk of prematurity (often iatrogenic)
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19
Q

ANAEMIA + PREGNANCY
What are the complications of iron deficiency anaemia?
How is it managed?

A
  • LBW + preterm delivery
  • Ferrous sulfate 200mg TDS
  • If not anaemic but low ferritin indicating iron stores then start them on it
  • Vitamin C can increase absorption of iron
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20
Q

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

A
  • Previous PROM/preterm
  • Smoking
  • Polyhydramnios
  • Amniocentesis
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21
Q

STAGES OF LABOUR
What are 7 important hormones in labour?

A
  • Prostaglandins
  • Oxytocin
  • Oestrogen
  • Beta-endorphins
  • Adrenaline
  • Prolactin
  • Relaxin
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22
Q

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

A
  • Engagement + descent
  • Flexion
  • Internal rotation
  • Extension (crowning)
  • Restitution/external rotation
  • Expulsion
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23
Q

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

A
  • Cervical dilation – <1cm (0), 1-2 (1), 3-4 (2), >5cm (3)
  • Cervical consistency – firm (0), intermediate (1), soft (2)
  • Cervical effacement –<30% (0), 40-50 (1), 60-70 (2), 80% (3)
  • Cervical position – posterior (0), intermediate (1), anterior (2)
  • Foetal station – –3 (0), -2 (1), -1/0 (2), ≥1 (3)
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24
Q

BREECH
What are the 3 types of breech presentation?

A
  • Extended (Frank) = most common, hips flexed, both legs extended with feet by head, buttocks presenting
  • Flexed (Complete) = hips + knees flexed so buttocks + feet presenting (Cannonballing)
  • Footling = one leg flexed, one extended, foot hanging through cervix
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25
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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26
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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27
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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28
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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29
Q

HYPEREMESIS
What are some associations of hyperemesis gravidarum?

A
  • nulliparity,
  • hyperthyroid,
  • obesity,
  • decreased in smokers
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30
Q

HYPEREMESIS
How is severity assessed?

A

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

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31
Q

ANAEMIA + PREGNANCY
What are some causes?

A

Physiological,
Fe deficiency (increased demand),
B12 or folate deficiency

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32
Q

ANAEMIA + PREGNANCY
What are some risk factors?

A

Menorrhagia,
malaria,
hookworm,
twins,
poor diet

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33
Q

HELLP
what other condition is HELLP associated with?

A
  • 10% have antiphospholipid syndrome
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34
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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35
Q

SICKLE CELL DISEASE IN PREGNANCY
what are the risks of sickle cell disease during pregnancy?

A
  • Crises are more common during pregnancy
  • Increased risk of pre-eclampsia
  • Increased risk of delivery by CS due to fetal distress
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36
Q

SICKLE CELL DISEASE IN PREGNANCY
what are the foetal risks in sickle cell disease?

A
  • miscarriage
  • IUGR
  • prematurity
  • stillbirth
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37
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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38
Q

FOETAL HYDROPS
what is the pathophysiology?

A

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

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39
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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40
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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41
Q

LOW BIRTH WEIGHT
what are the risk factors for low birth weight?

A

➢ Low socioeconomic
➢ History of abuse
➢ Age (<15 or >35)
➢ Race (black, ethnic minorities…)

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42
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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43
Q

UTEROPLACENTAL INSUFFICIENCY
what are the investigations?

A

➢ USS
➢ Maternal alpha fetoprotein levels
➢ CTG

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44
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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45
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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46
Q

CHLAMYDIA IN PREGNANCY
what are the risks of chlamydia infection during pregnancy?

A
  • preterm labour
  • PROM
  • low birth weight
  • infection during delivery (conjunctivitis and pneumonia)
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47
Q

GONORRHOEA IN PREGNANCY
what are the risks?

A
  • miscarriage
  • premature birth
  • low birth weight
  • PROM
  • chorioamnionitis
  • eye infection in newborn
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48
Q

SYPHILIS IN PREGNANCY
what are the risks?

A

congenital syphilis
- premature births
- still births
- multi-organ problems to brain, eyes, heart, skin, teeth and bones

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49
Q

TRICH VAGINALIS IN PREGNANCY
what are the risks?

A
  • PROM
  • preterm births
  • low birth weight
  • female newborns can acquire infection during birth
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50
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
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51
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
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52
Q

CEPHALOPELVIC DISPROPORTION
what can increase the risk?

A
  • flat (platypelloid) pelvic opening
  • heart-shaped (android) pelvis
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53
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)
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54
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
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55
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)
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56
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)
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57
Q

PCOS
What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism
  • Insulin resistance
  • Oligo or amenorrhoea + sub/infertility
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58
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

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59
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)
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60
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
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61
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)
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62
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)
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63
Q

CERVICAL CANCER
What are some risk factors for cervical cancer?

A
  • Increased risk of catching HPV = early (unsafe) sex, lots of sexual partners
  • Smoking (limits availability to clear HPV)
  • HIV
  • COCP
  • High parity
  • Previous CIN/abnormal smear or FHx
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64
Q

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

A
  • Cervical intra-epithelial neoplasia (CIN)
  • CIN I = mild, affects 1/3 thickness of epithelial layer, likely to return to normal without Tx
  • CIN II = mod, affects 2/3 thickness of epithelial layer, likely to progress to cancer without Tx
  • CIN III or cervical carcinoma in situ = severe, v likely to progress to cancer without Tx
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65
Q

OVARIAN CANCER
What are some types of epithelial cell tumours?

A
  • Serous carcinoma (#1)
  • Endometrioid, clear cell, mucinous + undifferentiated tumours too
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66
Q

OVARIAN CANCER
What are sex-cord stromal tumours?

A
  • Arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles)
  • Sertoli-Leydig + granulosa cell tumours
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67
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)

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68
Q

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

A
  • COCP
  • Early menopause
  • Breast feeding
  • Childbearing
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69
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
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70
Q

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

A
  • Endometriosis
  • Fibroids + adenomyosis
  • Pelvic infection
  • Pregnancy
  • Benign cysts
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71
Q

OVARIAN CYST
What are the three types of functional cysts?

A
  • Follicular (most common)
  • Corpus luteum
  • Theca lutein
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72
Q

OVARIAN CYST
What are theca lutein cysts?
Association?

A
  • Stimulates growth of follicular theca cells so usually bilateral as resting follicles on both sides
  • Overstimulation of hCG (multiple + molar pregnancy as hCG v high)
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73
Q

OVARIAN CYST
What are the 2 benign epithelial neoplasms?

A
  • Serous cystadenoma (most common epithelial tumour)
  • Mucinous cystadenoma
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74
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)
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75
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
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76
Q

OVARIAN CYST
What are the germ cell tumour markers?

A
  • Lactate dehydrogenase
  • Alpha-fetoprotein
  • Human chorionic gonadotropin
77
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
78
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)

79
Q

ENDOMETRIAL CANCER
What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking (Seem to have anti-oestrogenic effect)
80
Q

ENDOMETRIAL POLYP
What are some risk factors of endometrial polyps?

A
  • Being peri or post-menopausal
  • HTN
  • Obesity
  • Tamoxifen
81
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
82
Q

VULVAL CANCER
What is the management of VIN?

A
  • Biopsy to Dx
  • Watch + wait with close follow up
  • Wide local excision to surgically remove lesion
  • Imiquimod cream or laser ablation
83
Q

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

A
  • UKMEC1 = barrier, IUS/IUD, POP, long-acting progesterone (<45), sterilisation
  • UKMEC2 = COCP after 40 used until 50, try ones with levonorgestrel or norethisterone as lower VTE risk
  • They don’t but may mask Sx
84
Q

MENOPAUSE
What is the mechanism of action of clonidine?

A
  • Alpha-adrenergic receptor agonist
85
Q

HRT
What are the side effects associated with oestrogen?

A
  • Nausea,
  • bloating,
  • headaches,
  • breast swelling or tenderness,
  • leg cramps
86
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
87
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
88
Q

URINARY INCONTINENCE
What causes urge incontinence/OAB?

A
  • Overactivity + involuntary contractions of the detrusor muscle
89
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
90
Q

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

A
  • Age
  • BMI
  • Multiparity (vaginal)
  • Spina bifida
  • Pelvic surgery
  • Menopause
91
Q

PREMENSTRUAL SYNDROME
What specialist management can be given for PMS?

A
  • Continuous transdermal oestrogen with progestogens
  • GnRH analogues if severe (add HRT to mitigate osteoporosis risk)
  • Hysterectomy + bilateral oophorectomy to induce menopause if severe
  • Danazol + tamoxifen for cyclical breast pain
  • Spironolactone for breast swelling + bloating
92
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
93
Q

ASHERMAN’S SYNDROME
What causes Asherman’s syndrome?

A
  • Pregnancy-related dilatation + curettage procedures
  • After uterine surgery
  • Pelvic infection like endometritis
94
Q

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

A
  • Secondary amenorrhoea
  • Infertility
  • Significantly lighter periods
  • Dysmenorrhoea
95
Q

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

A
  • Hysterosalpingography = contrast injected into uterus + XR
  • Sonohysterography = uterus filled with fluid + pelvic USS
  • Hysteroscopy gold standard + can dissect adhesions (recurrence after common)
96
Q

HRT
What are the side effects associated with progesterone?

A

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

97
Q

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

A

Hysterectomy or sacrohysteropexy

98
Q

HYDATIDIFORM MOLE
What is a complete mole?

A
  • Diploid trophoblast cells
  • Empty egg + sperm that duplicates DNA (all genetic material comes from father)
  • No foetal tissue
99
Q

HYDATIDIFORM MOLE
What is a partial mole?

A
  • Triploid (69XXX, 69XXY) trophoblast cells
  • 2 sperm fertilise 1 egg
  • Some recognisable foetal tissue
100
Q

HYDATIDIFORM MOLE
What are some risk factors for hydatidiform mole?

A
  • Extremes of reproductive age
  • Previous molar pregnancy
  • Multiple pregnancies
  • Asian women
  • OCP
101
Q

HYDATIDIFORM MOLE
What is the management of hydatidiform mole after evacuation?

A
  • Check urinary pregnancy test in 3w – if high or mets may need chemo (cisplatin)
  • Effective contraception as advised to avoid pregnancy for 12m
102
Q

PELVIC INFLAMMATORY DISEASE
What are some risk factors for PID?

A
  • Not using barrier contraception
  • Multiple sexual partners
  • Intrauterine device
  • Younger age
  • Existing STIs
  • Previous PID
103
Q

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

A
  • Pus cells on swabs from vagina or endocervix
  • Absence is useful to exclude PID
104
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)
105
Q

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

A

Gardnerella vaginalis,
H. influenzae,
E. coli.

106
Q

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

A

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

107
Q

GENITAL TRACT FISTULA
what are the different types?

A

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

108
Q

GENITAL TRACT FISTULA
what are the risk factors for genital tract fistulas?

A

➢ Childbirth
➢ Surgery
➢ Infection
➢ IBD
➢ Radiation

109
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

110
Q

OVERACTIVE BLADDER
what are the risk factors for overactive bladder?

A

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

111
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
112
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
113
Q

SYPHILIS
What is a potential adverse effect of treating syphilis?

A
  • Jarisch-Herxheimer reaction within a few hours of treatment
  • Fever, rash + tachycardia thought to be due to release of endotoxins following bacterial death
114
Q

GENITAL WARTS
How is genital warts managed?

A
  • Prophylaxis with HPV vaccine for 12–13y (may be given to MSM, trans men/women + sex workers)
  • Topical podophyllotoxin cream/lotion or cryotherapy.
  • GUM contact tracing, contraceptive advice
115
Q

HIV
What is HIV?
What is the pathophysiology of HIV?

A
  • RNA retrovirus that encodes reverse transcriptase
  • Binds to GP120 envelope glycoprotein to CD4 receptors which migrate to lymphoid tissue where virus replicates + produces billions of new virions
  • Reverse transcriptase makes single strand RNA > double stranded DNA + viral DNA is integrated to host cell’s DNA with enzyme integrase + core viral proteins synthesised + cleaved by viral protease
  • These then released + in turn infect new CD4 cells
116
Q

HIV
What tests can be used to investigation HIV?

A
  • Serum/salivary HIV enzyme-linked immunosorbent assay (ELISA)
  • Rapid point of care screening blood test for HIV antibodies
  • PCR testing
117
Q

HIV
Explain the process of HIV ELISA

A

Can take 3m for HIV Ab detection so confirmatory assay after 3m.

118
Q

HIV
What is the generic management for HIV?
What is the standard therapy?
What is the aim of therapy?

A
  • Specialist HIV, infectious diseases + GUM clinics
  • Highly active anti-retrovirus therapy (HAART) with 2 NRTIs + third agent
  • Goal to achieve normal CD4 count + undetectable viral load
119
Q

HIV
What are the 4 main groups of HIV treatment?

A
  • Nucleoside reverse transcriptase inhibitors (NRTIs)
  • Protease inhibitors (PIs)
  • Integrase inhibitors (IIs)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
120
Q

HIV
What are some examples of and the mechanism of action of…

i) NRTIs?
ii) PIs?
iii) IIs?
iv) NNRTIs?

A

i) Zidovudine, tenofovir, emtricitabine – inhibits synthesis of DNA by reverse transcriptase
ii) Indinavir (end –navir) – acts competitively on HIV enzyme involved in production of functional viral proteins
iii) Raltegravir (end –gravir) – inhibits insertion of HIV DNA to genome
iv) Nevirapine – binds directly to + inhibits reverse transcriptase

121
Q

SYPHILIS
What is the causative organism?

A

Treponema pallidum – spirochete (spiral-shaped) bacteria

122
Q

CANDIDIASIS
What are some risk factors?

A

Increased oestrogen (pregnancy, during menstrual years)
poorly controlled DM,
immunosuppression,
broad spectrum Abx

123
Q

LYMPHOGRANULOMA VENEREUM
what is it?

A

STI caused by serovars L1, L2 or L3 or chlamydia trachomatis

124
Q

LYMPHOGRANULOMA VENEREUM
what are the clinical features?

A

Painless genital ulcer
Appears 3-12 days after infection
May not be noticeable e.g. if occurs inside the vagina
Inguinal lymphadenopathy
Proctitis, rectal pain, rectal discharge (in rectal infections)
Systemic symptoms such as fever and malaise

125
Q

LYMPHOGRANULOMA VENEREUM
what is the management?

A

Treatment is with antibiotics. Common regimes include:

Oral doxycycline 100 mg twice daily for 21 days
Oral tetracycline 2 g daily for 21 days
Oral erythromycin 500 mg four times daily for 21 days

126
Q

CHANCROID
what are the causes?

A

Haemophilus ducreyi

Given its relatively high incidence in topical areas and Greenland, it is important to inquire in the history about recent travel.

127
Q

CHANCROID
what are the clinical features?

A

A painful genital lesion which may bleed on contact
Associated symptoms include painful lymphadenopathy

128
Q

CHANCROID
what is the management?

A

The infection is treated using antibiotics (typically Ceftriaxone, Azithromycin or Ciprofloxacin)

129
Q

COCP
What pill is recommended…
i) as first line?
ii) in PMS?
iii) in acne + hirsutism?

A

i) Pills with levonorgestrel or noresthisterone (microgynon or Leostrin) as lower VTE risk.
ii) Pills containing drospirenone as anti-mineralocorticoid + anti-androgen activity can help Sx (esp. w/ continuous use).
ii) Pills containing cyproterone acetate (co-cyprindiol) as anti-androgen effects but the oestrogenic effects give it higher VTE risk so usually stopped after 3m when Sx reduced.

130
Q

COCP
What are the benefits of the COCP?

A
  • Effective contraception, rapid return of fertility after stopping.
  • Improvement in PMS, menorrhagia + dysmenorrhoea (acne in some).
  • Reduced risk of endometrial, ovarian, colon cancer + benign ovarian cysts.
131
Q

COCP
What are some side effects + risks with the COCP?

A
  • Unscheduled bleeding common in first 3m.
  • Breast pain + tenderness.
  • Mood changes + depression.
  • Headaches, HTN, VTE.
  • Small raise in risk of breast + cervical cancer (risk normalises after 10y taking pill).
  • Small raise in risk of MI + stroke.
132
Q

COCP
What are the UKMEC4 criteria for the COCP?

A
  • Uncontrolled HTN.
  • Migraine with aura.
  • > 35 smoking >15/day.
  • Major surgery with prolonged immobility (stop 4w before major surgery)
  • Hx of stroke, IHD, AF, VTE.
  • Active breast cancer.
  • Liver cirrhosis or tumours.
  • SLE + antiphospholipid syndrome.
  • Breastfeeding before 6w postpartum (UKMEC2 after).
133
Q

COCP
What are the UKMEC3 criteria for the COCP?

A
  • > 35 smoking <15/day.
  • BMI >35kg/m^2.
  • Controlled HTN.
  • VTE FHx in 1st degree relatives.
  • Immobility.
  • Known carrier of BRCA1/2.
134
Q

POP
What different types of POP are there and what are their mechanisms?

A

Traditional POP (norgeston) –
- Thickens cervical mucus.
- Alters endometrium so less accepting of implantation.
- Reduced ciliary action in fallopian tube.
Desogestrel POP (Cerazette) –
- Inhibits ovulation (main mechanism) + above.

135
Q

POP
What is the main complaint/side effect of the POP?
What are some other side effects of the POP?

A
  • Unscheduled bleeding common in first 3m (if persists exclude other causes like STIs, pregnancy, cancer).
  • Changes to bleeding schedule one of primary adverse effects (40% regular bleeding, 40% irregular, prolonged or troublesome + 20% amenorrhoeic).
  • Breast tenderness, headaches + acne.
136
Q

POP
What are some risks of the POP?

A
  • Increased risk of ovarian cysts, small risk of ectopic pregnancy with traditional POP due to reduced ciliary action, minimal increased risk of breast cancer (returns to normal 10y after stopping).
137
Q

PROGESTERONE INJECTION
What is the mechanism of action of the progesterone injection?

A
  • Inhibits ovulation by inhibiting FSH secretion by the pituitary gland + prevents development of follicles in the ovary.
  • Thickens cervical mucus + alters endometrium to make it less favourable for implantation.
138
Q

PROGESTERONE INJECTION
What are 3 unique side effects to the progesterone injection?

A
  • Weight gain
  • Reduced BMD (oestrogen maintains BMD + mostly produced by follicles in ovaries)
    – Makes depot unsuitable for those >45
  • Takes 12m for fertility to return after stopping
139
Q

PROGESTERONE INJECTION
What are some general side effects of the progesterone injection?

A
  • Acne.
  • Reduced libido.
  • Mood issues (depression).
  • Headaches.
  • Alopecia.
  • Skin reactions at injection sites.
  • Small rise in breast/cervical cancer risk.
140
Q

PROGESTERONE INJECTION
What are the UKMEC3 + 4 criteria for progesterone injection?

A
  • UKMEC4 = active breast cancer.
  • UKMEC3 = IHD + stroke, unexplained vaginal bleeding, severe liver cirrhosis + liver cancer.
141
Q

PROGESTERONE IMPLANT
What is the mechanism of action for the progesterone implant?

A
  • Inhibits ovulation.
  • Thickens cervical mucus.
  • Alters endometrium to make it less accepting to implantation.
142
Q

PROGESTERONE IMPLANT
What are the pros of progesterone implant?

A
  • Effective + reliable.
  • Can improve dysmenorrhoea + can make periods lighter or stop altogether.
  • No weight gain, effect on BMD, no VTE risk, no restrictions for obese patients.
143
Q

PROGESTERONE IMPLANT
What are the side effects of the progesterone implant?

A
  • Problematic bleeding (20% amenorrhoeic, 25% frequent/prolonged bleeding, 33% infrequent, rest normal, can use COCP for 3m if problematic bleeding + no C/Is).
  • Can worsen acne, no STI protection.
144
Q

COILS
What are the risks of coil insertion?

A
  • Insertion risks (bleeding, pain on insertion [use NSAIDs],
  • vasovagal reactions,
  • uterine perforation,
  • PID + expulsion rate highest in first 3m.
145
Q

COILS
What are the contraindications to the coils?

A
  • PID or infection,
  • immunosuppression,
  • pregnancy,
  • unexplained bleeding,
  • pelvic cancer,
  • uterine cavity distortion (fibroids).
146
Q

COILS
What are the drawbacks of the IUD?

A
  • Procedure with risks for insertion/removal.
  • Can cause HMB/IMB which often settles.
  • Some women have pelvic pain.
  • No STI protection.
  • Increased risk of ectopic pregnancies.
  • Occasionally falls out.
147
Q

COILS
What is the mechanism of action for the IUS?

A
  • Progesterone component thickens cervical mucus.
  • Alters endometrium making less hospitable + inhibits ovulation in small # of women.
148
Q

COILS
What are the benefits of the IUS?

A
  • Can make periods lighter or stop.
  • May improve dysmenorrhoea or pelvic pain related to endometriosis.
  • No effect on BMD, VTE, no restrictions in obese pts.
149
Q

COILS
What are the drawbacks of the IUS?

A
  • Procedure with risks for insertion/removal.
  • Can cause spotting or irregular bleeding.
  • Some women experience pelvic pain.
  • No STI protection.
  • Increased risk of ectopic pregnancies.
  • Occasionally falls out.
  • Increased incidence of ovarian cysts.
  • Systemic absorption can lead to progesterone Sx (acne, headaches, breast tenderness).
150
Q

EMERGENCY CONTRACEPTION
For the copper IUD, what are the pros and cons?

A

Pros
- Choice not affected by BMI, enzyme-inducing drugs or malabsorption.
- Can leave in as long-term contraceptive
Cons
- PID (especially if STIs)
- Normal risks with coil insertion

151
Q

EMERGENCY CONTRACEPTION
For Ulipristal acetate, answer the following…
i) dose?
ii) effectiveness?
iii) time frame?
iv) mechanism?
v) extra notes?
vi) side effects?

A

i) Single 30mg dose
ii) Second most effective but decreases with time
iii) <120h
iv) Selective progesterone receptor modulator that inhibits ovulation
v) Vomiting within 3h then repeat dose
vi) Spotting + changes to next menstrual period, abdo/pelvic/back pain, mood changes, headaches, dizziness, breast tenderness

152
Q

EMERGENCY CONTRACEPTION
For Ulipristal acetate, what are the pros and cons?

A

Pros
- More effective than levonorgestrel
- Can be used >1 in one cycle
Cons
- Avoid breastfeeding for 1w (express but discard)
- Avoid in severe asthma
- Wait 5d before starting COCP or POP with 7 or 2d extra contraception needed

153
Q

EMERGENCY CONTRACEPTION
For levonorgestrel, answer the following…
i) dose?
ii) effectiveness?
iii) time frame?
iv) mechanism?
v) side effects?

A

i) Single 1.5mg dose (3mg if BMI >26kg/m^2)
ii) Least effective of group 84%
iii) <72h
iv) Stops ovulation + inhibits implantation
v) Spotting + changes to next menstrual period, diarrhoea, breast tenderness, dizziness, depressed mood

154
Q

EMERGENCY CONTRACEPTION
For Levonorgestrel, what are the pros and cons?

A

Pros
- Safe during breastfeeding (Avoid for 8h to avoid infant exposure though).
- COCP/POP can start instantly but with extra contraception for 7/2d
- Use more than once in a menstrual cycle
Cons
- Less effective

155
Q

FEMALE INFERTILITY
In terms of causes of female infertility, what are disorders of ovulation?

A

PCOS
POI,
pituitary tumours,
hyperprolactinaemia,
Turner syndrome,
Sheehan’s,
previous radio/chemo

156
Q

FEMALE INFERTILITY
What are some risk factors of infertility?

A
  • Extremes of weight
  • Increasing age
  • Smoking
  • Alcohol/drug use
157
Q

FEMALE INFERTILITY
What are the ovarian reserve tests?

A
  • Serum FSH + LH on days 2–5 (high = poor ovarian reserve)
  • Anti-mullerian hormone (released by granulosa cells in growing follicles so falls as eggs depleted)
  • Antral follicle count on USS (Few suggest poor ovarian reserve)
158
Q

FEMALE INFERTILITY
How would you manage anovulation?

A
  • Weight loss
  • Clomiphene (selective oestrogen receptor modulator on days 2–6 to inhibit oestrogen + cause more GnRH + so FSH + LH release) or letrozole (aromatase inhibitor) to stimulate ovulation.
  • Gonadotrophins to stimulate ovulation if resistant to clomiphene
  • Ovarian drilling may be used in PCOS
159
Q

MALE INFERTILITY
In terms of male infertility, what are the pre-testicular causes?

A

Pituitary/hypothalamus pathology,
suppression due to stress,
chronic conditions,
hyperprolactinaemia,
Kallmann’s

160
Q

MALE INFERTILITY
In terms of male infertility, what are the genetic/congenital causes?

A

Klinefelter’s,
Y chromosome deletions

161
Q

MALE INFERTILITY
When managing male infertility, what are some management options?

A
  • Intrauterine insemination, IUI (collect + separate high-quality sperm + inject into uterus)
  • Intracytoplasmic sperm injection, ICSI (inject sperm directly into cytoplasm of egg + inject into uterus)
  • Surgical correction of an obstruction in the vas
162
Q

ASSISTED CONCEPTION
What are the risks and complication with IVF?

A
  • Multiple pregnancy
  • Miscarriage + ectopics
  • Ovarian hyperstimulation syndrome
  • Bleeding + infection at egg collection
  • Failure
163
Q

ASSISTED CONCEPTION
What is the clinical presentation of ovarian hyperstimulation syndrome?

A
  • Mild = abdo pain + vomiting
  • Mod = N+V + ascites on USS
  • Severe = ascites, oliguria
  • Critical = anuria, VTE, ARDS
164
Q

ASSISTED CONCEPTION
What are the risk factors for ovarian hyperstimulation syndrome?

A
  • Younger age.
  • Lower BMI.
  • PCOS.
  • Higher antral follicle count.
165
Q

ASSISTED CONCEPTION
What investigations would you do in ovarian hyperstimulation syndrome and what would they show?
How could you identify someone at risk?

A
  • Activation of RAAS > high renin
  • Haematocrit raised as less fluid in intravascular space
  • USS + serum oestrogen (high = risk) – monitor these to identify those at risk.
166
Q

ASSISTED CONCEPTION
How do you manage ovarian hyperstimulation syndrome?

A
  • PO fluids
  • Monitor urine output
  • LMWH
  • Paracentesis for ascites
  • IV colloids
167
Q

POP
What are the rules about UPSI in for the POP?

A

Sex since missing pill or within 48h of restarting = emergency contraception.

168
Q

FEMALE INFERTILITY
In terms of causes of female infertility, what are the tubal/uterine/cervical factors?

A

PID,
sterilisation,
Asherman’s,
fibroids,
polyps,
endometriosis,
uterine deformity

169
Q

MALE INFERTILITY
In terms of male infertility, what are the testicular causes?

A

Damage from mumps, undescended testes, trauma, cancer, radio/chemo

170
Q

MALE INFERTILITY
In terms of male infertility, what are the post-testicular causes?

A

Retrograde ejaculation,
scarring from epididymitis (chlamydia),
absence of vas deferens (may be associated with cystic fibrosis, even carriers),
damage to testicle or vas (trauma, surgery, cancer).

171
Q

MALE INFERTILITY
In terms of male infertility, what are the azoospermia causes?

A

Steroid abuse,
vasectomy

172
Q

MALE INFERTILITY
In terms of male infertility, what are the teratozoospermia causes?

A

Testicular cancer

173
Q

MALE INFERTILITY
How would you manage hormonal causes of infertility?

A
  • Gonadotrophins if hypogonadotrophic hypogonadism, bromocriptine if hyperprolactinaemia + sexual dysfunction
174
Q

BREAST CANCER
What tumour marker can be used to monitor response to breast cancer treatment and disease recurrence?

A
  • CA 15-3
175
Q

BREAST CANCER
What are some complications of breast cancer?

A
  • Locally advanced (rare), try shrink with radio, chemo, or hormone therapy to try operate, salvage surgery + stage for mets
  • Metastatic breast cancer (2Ls 2Bs) = Lungs, Liver, Bones, Brain
176
Q

BREAST CANCER
What adjuvant endocrine therapy may be given to women?

A
  • All ER+ve women need endocrine therapy as increases survival
  • Bisphosphonates to reduce rate of bone mets in ER+ve
  • Trastuzumab (Herceptin) used in HER2+ve + chemo
177
Q

BREAST INFECTION
What is the management of non-lactational mastitis?

A
  • Same as lactational mastitis (flucloxacillin or erythromycin) but + metronidazole
178
Q

GYNAECOMASTIA
What are some pathological causes of gynaecomastia?

A
  • Drugs (spironolactone, oestrogen, anabolic steroids)
  • Marijuana
  • Liver failure
  • Testicular failure or tumour (Can produce beta-hCG)
179
Q

METASTATIC BREAST CANCER
What is the management?

A
  • Bisphosphonates + denosumab, radio/chemo + Sx control
180
Q

BREAST CANCER
what is tamoxifen?

A

tamoxifen inhibits the oestrogen receptor on breast cancer cells
It increases survival by 15-25% in woman with ER+ cancer
give for 10 years in higher risk women

181
Q

BREAST CANCER
what are the complications of tamoxifen?

A

hot flushes
nausea
vaginal bleeding
rarely thrombosis and endometrial cancer

182
Q

BREAST CANCER
what are aromatase inhibitors?

A

letrozole
Inhibit aromatase enzyme responsible for the conversion of androgens to oestogen in post-menopausal woman
slightly better anticancer efficacy than tamoxifen

183
Q

BREAST CANCER
what are the side effects of aromatase inhibitors?

A

hot flushes
reduced bone density
joint pains

184
Q

BREAST CANCER
how is HER-2 breast cancer managed?

A

Currently 1 year of 3 weekly adjuvant Trastuzumab given alongside chemotherapy (usually FEC-T).

185
Q

PAGET’S DISEASE OF THE NIPPLE
what are the risk factors?

A
  • old age
  • FHx of breast cancer
  • Previous breast cancer
  • overweight
  • excess alcohol
  • smoking
  • risk factors for breast cancer
186
Q

PAPILLOMA
what is the clinical presentation?

A
  • bloody or clear discharge from a single duct
187
Q

PAPILLOMA
what is the management?

A
  • removal via vacuum assisted excision (VAE)
188
Q

PAPILLOMA
what are they associated with?

A

atypical hyperplasia - this increases the risk of developing breast cancer

189
Q

ANAEMIA IN PREGNANCY
What is the cut off for Hb in first trimester?
What is the cut off for Hb in second/third trimester?
What is the cut off for Hb postpartum?

A

first trimester - <110g/l
second/third trimester - <105g/l
postpartum - <100g/l

B TO REVISE - PHASE 3A (9 decks)

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