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A TO REVISE - PHASE 3A > OBSTETRICS TO DO > Flashcards

OBSTETRICS TO DO Flashcards

1
Q

ECTOPIC PREGNANCY
Where is the most common site for an ectopic?
What is the most common site for a ruptured ectopic?

A
  • Ampulla
  • Isthmus
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2
Q

ECTOPIC PREGNANCY
What is expectant management?
What are the indications?
What indicates that it has worked?

A
  • Effectively do nothing
  • Clinically stable (no Sx), ectopic <35mm, no heartbeat, serum hCG <1000IU/L (consider up to 1500) + able to return for follow up
  • Serum hCG days 2, 4 + 7 (drop ≥15% then repeat weekly until negative)
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3
Q

ECTOPIC PREGNANCY
What is medical management?
What are the indications?
What indicates that it has worked?

A
  • Single dose IM 50mg/m^2 methotrexate
  • No significant pain, unruptured ectopic <35mm, no heartbeat, serum hCG <1500 (consider up to 5000IU/L) + able to return for follow up
  • hCG levels at days 4 + 7 then weekly, <15% fall = ?another dose
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4
Q

ECTOPIC PREGNANCY
What are the requirements for methotrexate management?
What are some side effects?

A
  • Satisfactory liver + renal functions
  • Teratogenic so effective contraception for 3m
  • Conjunctivitis, diarrhoea, abdo pain + stomatitis
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5
Q

MISCARRIAGE
What are some other causes of miscarriage?

A
  • PCOS
  • TORCH infections
  • Iatrogenic (amniocentesis, CVS)
  • Smoking, substance abuse
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6
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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7
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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8
Q

TERMINATING PREGNANCY
What is the legal framework for terminating pregnancies?

A
  • 1967 Abortion Act (+ 1990 amendment which reduced gestation from 28 to 24w)
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9
Q

ANTENATAL SCREENING
What results indicate higher risk for…

i) nuchal translucency?
ii) beta-hCG?
iii) PAPP-A?

What else is taken into account?

A

i) >6mm
ii) Higher result
iii) Lower result

  • Maternal age, USS crown rump length, detection rate 85%
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10
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

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11
Q

ANTENATAL SCREENING
What risk score would warrant further invasive tests?
What are those tests?

A
  • > 1:150 = screen +ve
  • Amniocentesis
  • Chorionic villus sampling (CVS)
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12
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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13
Q

ADHERED PLACENTA
What are some risk factors for a morbidly adhered placenta?

A
  • Previous c-sections (placenta attaches to site)
  • Myomectomy
  • Surgical TOP
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14
Q

VASA PRAEVIA
What are some risk factors for vasa praevia?

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

PRE-ECLAMPSIA
What are the signs of pre-eclampsia?

A
  • Raised BP + proteinuria are hallmarks
  • Rapid weight gain, RUQ tenderness
  • Ankle clonus (brisk reflexes normal in pregnancy but not clonus)
  • Papilloedema if severe
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23
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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24
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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25
Q

PRE-ECLAMPSIA
What are the 2 big complications of pre-eclampsia?

A
  • Eclampsia
  • HELLP syndrome
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26
Q

PRE-ECLAMPSIA
What is the criteria for outpatient management of pre-eclampsia?
What care is given?

A
  • BP <160/110, no or low proteinuria (≤+, <0.3g/24h) + no symptoms
  • Weekly review of bloods, twice weekly mother + foetal evaluation (HBPM + urine)
  • Any changes > hospital
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27
Q

IUGR
What are the two types of IUGR?

A
  • Symmetrical = entire body is proportionately small, tends to be seen in early onset IUGR, TORCH + chromosomal abnormalities
  • Asymmetrical = undernourished foetus that is compensating by directing most of its energy to maintain growth of vital organs like brain + heart
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28
Q

IUGR
What might be seen in asymmetrical IUGR?

A

Head-sparing effect –
- Normal head size but small abdominal circumference + thin limbs
- Mostly secondary to placental insufficiency

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29
Q

IUGR
What is low birth weight?

A
  • Baby born with a weight <2.5kg (regardless of gestational age)
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30
Q

IUGR
What are the 3 broad categories causing IUGR?

A
  • Placental insufficiency (most common cause)
  • Maternal factors
  • Foetal factors
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31
Q

IUGR
What are some placental causes of IUGR?

A
  • Abnormal trophoblast invasion (pre-eclampsia, placenta accreta)
  • Infarction, abruption, location (praevia)
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32
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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33
Q

IUGR
What are some complications of IUGR?

A
  • Hypoglycaemia
  • Risk of necrotising enterocolitis
  • Neonatal jaundice
  • Hypothermia
  • Respiratory issues
  • Long-term sequelae include T2DM, HTN, obesity, behavioural problems, CP
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34
Q

IUGR
What causes…

i) hypoglycaemia?
ii) necrotising enterocolitis?
iii) neonatal jaundice?

A

i) Blood directed away from liver>brain so glycogen stores don’t develop adequately
ii) Reduced blood to bowel
iii) Compensatory polycythaemia for reduced oxygen supply from mother if reduced placental perfusion

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35
Q

IUGR
What causes…

i) hypothermia?
ii) respiratory problems?

A

i) No fat stores developed so cannot thermoregulate, large surface area
ii) Kidney hypoperfusion > decreased urine output > oligohydramnios > inadequate lung development

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36
Q

IUGR
What are the investigations for IUGR?

A
  • BP + urine dipstick (?pre-eclampsia)
  • Karyotyping (?foetal)
  • Infection screen, TORCH (?infection)
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37
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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38
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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39
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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40
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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41
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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42
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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43
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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44
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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45
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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46
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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47
Q

ANAEMIA + PREGNANCY
What is the management of macrocytic anaemias?

A
  • Pernicious = IM hydroxocobalamin
  • B12 deficiency = B12 tablets (cyanocobalamin)
  • Folate = increased from 400mcg to 5mg/day to reduce NTD.
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48
Q

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

A
  • Previous PROM/preterm
  • Smoking
  • Polyhydramnios
  • Amniocentesis
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49
Q

STAGES OF LABOUR
What are 7 important hormones in labour?

A
  • Prostaglandins
  • Oxytocin
  • Oestrogen
  • Beta-endorphins
  • Adrenaline
  • Prolactin
  • Relaxin
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50
Q

STAGES OF LABOUR
What is the first stage of labour?
How is it further divided?

A
  • From onset of labour (true contractions) until the cervix is fully dilated
  • Latent phase = from 0–3cm dilation
  • Active phase = from 3–10cm
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51
Q

STAGES OF LABOUR
What is the difference between latent and active phase of the first stage of labour?

A
  • Latent: cervix begins to efface, irregular contractions, ‘show’, can last 2–3d (usually 6h)
  • Active: stronger, more regular contractions (4:10), cervix continues effacing
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52
Q

STAGES OF LABOUR
What is the second stage of labour?
How is it further divided?

A
  • From full dilation to delivery of the foetus
  • Passive stage: complete dilation but no pushing (often 1 hour)
  • Active stage: maternal pushing until delivery
53
Q

STAGES OF LABOUR
What is considered a delay in the active second stage of labour?
What does success depend on?

A
  • > 2h in nulliparous, 1h in multiparous
  • 3Ps (power, passenger + passage [?Psyche of mum])
54
Q

STAGES OF LABOUR
What are the parts of the APGAR score?

A

Activity – absent 0, flexed arms + legs 1, active 2
Pulse – absent 0, <100bpm 1, >100bpm 2
Grimace – floppy 0, minimal response to stimulation 1, prompt response to stimulation 2
Appearance – blue 0, blue extremities 1, pink 2
Respiration – absent 0, slow + irregular 1, vigorous cry 2

55
Q

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

A
  • Engagement + descent
  • Flexion
  • Internal rotation
  • Extension (crowning)
  • Restitution/external rotation
  • Expulsion
56
Q

STAGES OF LABOUR
What is engagement?

A
  • Passage of presenting part into pelvic inlet
  • Entire head felt = 5/5ths palpable aka not engaged
  • Unable to feel head = 0/5ths palpable aka fully engaged
  • Foetus is engaged when >50% of presenting part descended into pelvis
57
Q

STAGES OF LABOUR
What is descent?
How can descent be described?
What is descent encouraged by?

A
  • Downward passage of presenting part through bony pelvis
  • Position of baby’s head (cm) in relation to mother’s ischial spines
  • Increased abdo muscle tone and increased frequency + strength of contractions
58
Q

STAGES OF LABOUR
How can descent of the baby be described?

A

In relation to ischial spines in cm –
- –5 = baby high up at around the pelvic inlet
- 0 = head at ischial spines (engaged)
- +5 = foetal head descended further out

59
Q

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

A
  • Occiput transverse
60
Q

STAGES OF LABOUR
What is flexion?

A
  • Uterine contractions exert pressure down foetal spine towards occiput + cause neck flexion, allowing circumference of foetal head to reduce
61
Q

STAGES OF LABOUR
What is internal rotation?
Why does it occur?

A
  • Foetus passively internally rotates from OT to OA/OP to allow shoulders to negotiate pelvic inlet
  • Pelvic inlet widest diameter is transverse (side-side)
62
Q

STAGES OF LABOUR
What is extension?

A
  • Foetal occiput slips beneath suprapubic arch allowing head to extend + foetal head is born, usually facing maternal back (occiput anterior)
63
Q

STAGES OF LABOUR
What is restitution?

A
  • Shoulders only now negotiating pelvic outlet so head externally rotates to face mother’s L/R medial thigh so shoulders can pass
  • Pelvic outlet widest diameter is A-P (front-back)
64
Q

STAGES OF LABOUR
What is expulsion?
How may this be assisted?

A
  • Ultimately ends with delivery of foetus
  • Gentle downwards traction > deliver shoulder below suprapubic arch
  • Gentle upwards traction > deliver posterior shoulder (caution with excessive force as may cause brachial plexus damage)
65
Q

FAILURE TO PROGRESS
What are the 2 types of abnormal progression in labour?

A
  • Slow from beginning (primary dysfunctional labour) –may be insufficient uterine contractions
  • Sudden slowing of labour (secondary arrest) – may be cephalopelvic disproportion
66
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)
67
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
68
Q

CTG
How do you interpret a CTG?

A

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

69
Q

CTG
What might different foetal baseline rates tell you?

A
  • > 160 may be maternal pyrexia, prematurity, chorioamnionitis
  • <110 may be maternal beta-blockers, increased foetal vagal tone
70
Q

CTG
What are decelerations?
What are the 3 types and their causes?

A
  • Fall in baseline HR by 15 for ≥15s
  • Early = peak of contraction corresponds with trough of depression (head compression from uterine contraction = normal)
  • Late = deceleration after contraction (hypoxia = placental insufficiency, asphyxia)
  • Variable = vary in shape + timing (cord compression)
71
Q

CTG
What are the pros of CTGs?

A
  • Allows long-term monitoring
  • Can pick up on foetal distress
  • Can be on constantly to identify any slight changes
72
Q

CTG
What are the cons of CTGs?

A
  • No improvement in perinatal outcomes in low-risk pregnancies
  • Foetal exposure to USS ionisation
  • Ambulatory monitoring may not be possible
  • Doesn’t give true beat to beat FHR monitoring or morphological Ax of heart
73
Q

FOETAL ECG
What is an alternative to scalp ECG?

A
  • Abdominal foetal ECG
  • Can be used ambulatory at home but only for high risk, morphological analysis possible + non-invasive
74
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
75
Q

INSTRUMENTAL DELIVERY
What are the main risks of ventouse delivery?

A
  • 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
76
Q

C-SECTION
What are the different categories of c-section?

A
  • 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
77
Q

C-SECTION
What two types of anaesthesia can be used in c-sections?
What else is given in c-sections?

A
  • General
  • Regional block (spinal)
  • H2 receptor antagonists or PPIs, prophylactic Abx, oxytocin (PPH), LMWH for VTE prophylaxis
78
Q

PAIN RELIEF
What are some important notes about single shot opioids?

A
  • Lipid soluble so crosses placenta rapidly
  • Diamorphine 2x as potent as morphine so faster onset
  • Pethidine metabolites can cause seizures so avoid in epileptics
79
Q

PAIN RELIEF
What are some side effects from opioids?

A
  • Foetal = resp depression, diminishes breast seeking + feeding behaviour
  • Maternal = euphoria + dysphoria, N+V, can prolong 1st + 2nd stages, resp depression + pruritus
80
Q

PAIN RELIEF
What 4 regimes can be given for regional techniques?

A
  • Intermittent = high conc LA, labour intensive, periods of inadequate analgesia + haemodynamic instability
  • Continuous = low dose LA + opioid, less labour intensive, constant analgesia + haemodynamic stability
  • Continuous + bolus = greater maternal satisfaction
  • CSE = rapid onset, high satisfaction, reduced LA dose
81
Q

PAIN RELIEF
What medications can be given epidurally?

A
  • LA like bupivacaine
  • Opioids like fentanyl, diamoprhine
82
Q

PAIN RELIEF
What sequential effects do regional techniques have?

A
  • Autonomic (vasodilation = reduced MAP)
  • Sensory (analgesia)
  • Motor (motor blockade) + fever
83
Q

PAIN RELIEF
What are the indications for regional techniques?

A
  • Maternal request
  • HTN/pre-eclampsia
  • Cardiac disease
  • Induced labour
  • Multiple births
  • Instrumental/op delivery likely
84
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
85
Q

PERINEAL TEARS
How are third degree tears further classified?

A
  • 3A = <50% of external anal sphincter thickness torn
  • 3B = >50% of EAS thickness torn
  • 3C = EAS + internal anal sphincter torn
86
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
87
Q

MENTAL HEALTH
What are some red flags in terms of maternal mental health?

A
  • Recent change in mental state or new Sx
  • New thoughts or acts of violence/self-harm
  • New + persistent feelings of incompetency as mother or estrangement from baby
88
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
89
Q

HYPEREMESIS
What are some associations of hyperemesis gravidarum?

A
  • nulliparity,
  • hyperthyroid,
  • obesity,
  • decreased in smokers
90
Q

HYPEREMESIS
How is severity assessed?

A

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

91
Q

OBSTETRIC CHOLESTASIS
What are some associations?

A
  • Asian women, thought to be due to increased oestrogen + progesterone levels
92
Q

ANAEMIA + PREGNANCY
What are some causes?

A

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

93
Q

ANAEMIA + PREGNANCY
What are some risk factors?

A

Menorrhagia,
malaria,
hookworm,
twins,
poor diet

94
Q

STAGES OF LABOUR
How quickly are women expected to dilate during the active phase?

A
  • Primis = 0.5cm/h,
  • multiparous = 1cm/h
95
Q

UTERINE RUPTURE
What are the two types?

A
  • Incomplete = peritoneal lining surrounding uterus intact
  • Complete = peritoneal lining ruptures so uterine contents released into peritoneal cavity
96
Q

PPH
What are the secondary causes of PPH?

A

Secondary most common cause is retained placental tissue, endometritis

97
Q

HELLP
what other condition is HELLP associated with?

A
  • 10% have antiphospholipid syndrome
98
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

99
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
100
Q

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

A
  • miscarriage
  • IUGR
  • prematurity
  • stillbirth
101
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
102
Q

FOETAL HYDROPS
what are the different types?

A

immune and non-immune

103
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.

104
Q

FOETAL HYDROPS
what are the causes of immune foetal hydrops?

A

results from blood group incompatibility between the mother and the fetus causing fetal anaemia.
THIS IS RHESUS DISEASE OF THE NEWBORN**

105
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
106
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

107
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…)

108
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…)

109
Q

LOW BIRTH WEIGHT
what are the consequences of a low birth weight?

A

➢ Feeding struggles
➢ Respiratory distress syndrome
➢ Jaundice
➢ Infections
➢ PDA
➢ Intraventricular hemorrhage
➢ Retinopathy of prematurity, and hearing problems
➢ Intellectual and developmental disabilities
➢ Diabetes
➢ High blood pressure
➢ Heart disease
➢ Obesity

110
Q

LOW BIRTH WEIGHT
what is the management?

A

➢ IV fluids or gavage feeding
➢ Light therapy
➢ Supplemental surfactant or oxygen
➢ Surgery or medications (ROP or PDA), and for intraventricular hemorrhage
➢ Kangaroo care (skin to skin contact)
➢ Primary prevention: Avoid drinking, smoking and unhealthy diet during pregnancy. Get the flu vaccine

111
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

112
Q

UTEROPLACENTAL INSUFFICIENCY
what are the investigations?

A

➢ USS
➢ Maternal alpha fetoprotein levels
➢ CTG

113
Q

PUERPERAL INFECTION
what are the non-genital causes?

A
  1. Breast causes (mastitis, abscess)
  2. UTI (i.e., from catheter, hypotonic bladder, KEEPS bacteria)
  3. Thrombophlebitis (high risk of DVT and PE)
  4. Respiratory complications (mainly women with CS; due to atelectasis, aspiration, or bacterial pneumonia) – hence the need for prophylactic antibiotics before CS!
  5. Abdominal wound infection
114
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…)

115
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)
116
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)
117
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
118
Q

GONORRHOEA IN PREGNANCY
what are the risks?

A
  • miscarriage
  • premature birth
  • low birth weight
  • PROM
  • chorioamnionitis
  • eye infection in newborn
119
Q

GONORRHOEA IN PREGNANCY?
what is the management?

A

500mg ceftriaxone IM single dose

120
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

121
Q

SYPHILIS IN PREGNANCY
what is the management?

A

penicillin

122
Q

TRICH VAGINALIS IN PREGNANCY
what are the risks?

A
  • PROM
  • preterm births
  • low birth weight
  • female newborns can acquire infection during birth
123
Q

TRICH VAGINALIS IN PREGNANCY
what is the management?

A

metronidazole

124
Q

UTIs IN PREGNANCY
what are the treatments?

A
  • Oral antibiotics
    - Asymptomatic bacteriuria: 3 days
    - Cystitis 7 days
125
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.

126
Q

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

A

trimethoprim
it is a folate antagonist so can reduce folate levels

127
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
128
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
129
Q

CEPHALOPELVIC DISPROPORTION
what can increase the risk?

A
  • flat (platypelloid) pelvic opening
  • heart-shaped (android) pelvis

A TO REVISE - PHASE 3A (16 decks)

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