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Obs Med Flashcards

1
Q

Explain the effect of existing DM in pregnant women and the effect pregnancy has on DM?

A

Pregnancy on DM:

  • Insulin resistance INCREASES throughout pregnancy due to human placental lactogen and steroids (if insulin control gets better then means placenta isn’t working as well/check foetal movement and CTG)
  • Increased risk of severe hypoglycaemia (hypoglycaemia is more common in pregnancy) [therefore INCREASED metformin or insulin doses should be given in pregnancy]
  • Greater importance for tight glucose control
  • UTI risk increased
  • N+V, especially early on
  • Risk of deterioration of any nephropathy or retinopathy

DM on Pregnancy:

  • Increased risk of miscarriage and stillbirth
  • Increased risk of congenital malformation/spina bifida
  • Macrosomia risk
  • Increased risk of pre-eclampsia
  • IUGR
  • Increased operative delivery rate (CS) due to macrosomia/shoulder dystocia complications

A lot of these (PET, miscarriage etc) is due to poor implantation of the placenta

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2
Q

What pre-conception checks are important for women with DM?

A

Pre-conception:

  • Glucose control must be tight (use a 4h diary) and test HbA1c for risk level and then measure in 2nd and 3rd trimester –> >48mmol is a risk
  • Renal testing (U&Es, Cr)
  • BP checks
  • Retinal checks as retinopathy must be treated before pregnancy
  • Stop statin use
  • Start HIGH-dose folic acid (5mg OD) for first trimester (12wGA)
  • Changing medications to those that are safe in pregnancy (insulin, metformin + conservative measures)
  • Aspirin if at risk of PET
  • Counselling
  • -> Embryogenesis affected by DM so risk of miscarriage is higher
  • -> Poor glucose control harms baby (teratogenic - spina bifida)
  • -> Risks of polyhydramnios, growth restriction, stillbirth, infection
  • -> Macrosomia due to glucose passing to baby and they produce insulin, like IGF-1 a growth factor, causing increased growth
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3
Q

What is the management of DM women in pregnancy?

A

Antenatal:

  • Every 1-2w = joint antenatal diabetes clinics
  • Serial growth scans to monitor foetus (macrosmia/complications), every 4w from 28w [28->32w->36w
  • Strict CBG monitoring 4x/day, ensuring tight control with medications
  • Aspirin 75-150mg [150 if >70kg] to reduce PET risk
  • Folic acid varies [if BMI >30]
  • DM complications: Retinal scanning, once at booking and again in T2 + renal scans

Intrapartum:

  • 37+0 to 38+6w = induction or ELCS if growth scans are showing macrosomia BUT consider mums wishes [done earlier due to risk of stillbirth]
  • Consider active Mx of PPH due to increased risk [no use of Ergometrine in HTN!]
  • Neonates may be involved due to risk of neonatal hypoglycaemia/complications at birth

Postpartum:

  • DM tends to suddenly improve after giving birth and so make sure to monitor CBG and reduce insulin/medication doses
  • Safe to breastfeed on insulin+metformin
  • F/u in joint DM clinic
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4
Q

What are the ideal glucose monitoring measurements pregnant women should have?

A

CBG Monitoring should be done 4x a day = fasting and 3 post-prandial measurements:
- Fasting <5.4mmol/L (4-7)
- 1h post-prandial target <7.8mmmol/L
[- HbA1c may also used to assess risk]

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5
Q

What is GDM and what are risk factors for it?

A

GDM = new-onset diabetes during pregnancy which usually disappears after birth and occurs at around 24-28w gestation

Complications = same as DM in pregnancy but to a lesser degree due to reduced timeframe of glucose-induced effects

RFs:

  • BMI >30kg/m2
  • Previous GDM
  • Previous macrosomic baby (4.5/+ kg)
  • FHx of DM (1st degree)
  • Asian ethnicity
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6
Q

How would you Ix and Dx GDM?

A

Ix:

  • Urine dip –> if glycosuria –> 2h 75g OGTT immediately +/- HbA1c testing for pre-existing DM)
  • Previous GDM –> immediate 2h 75g OGTT and if normal, repeat at 24-28w)
  • Any RFs on clerking, but not prior GDM –> 2h 75g OGTT at 24-28w

Dx: [‘5,6,7,8’]

  • > Fasting plasma glucose > 5.6mmol/L
  • > 2h 75g OGTT > 7.8mmol/L
  • > If diagnosed, offer review at antenatal-DM clinic within 1w
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7
Q

How would you manage GDM?

A

Mx = similar as DM

1st line [if fasting glucose <7mmol/L]
-> 2w trial of conservative changes i.e. diet and exercise (CDE) advice, regular exercise such as walking, refer to dietician for low glycemic index food advice

2nd line [if targets not met by 2w and <7mmol/L]

  • > Metformin and CDE
  • > If metformin is contraindicated/unacceptable, then go to insulin

3rd line [if 2nd line ineffective OR FG >7mmol/L OR 6-6.9 with complications]

  • > Insulin alone if >7mmol at diagnosis or 6-6.9 with complications e.g. macrosomia
  • > Insulin + metformin + CDE if 3rd line

4th line
-> Consider glibenclamide for those who decline insulin and metformin doesn’t work/cannot tolerate it

PLUS:

  • Regular monitoring - 4x daily [fasting + 3x postprandial] aiming for <5.4 and <7.8mmol
  • Scans every 4w from 28w
  • HbA1c monitoring also used during pregnancy
  • Advise on delivery –> offer IOL or ELCS between 37-38+6w but no later than 40+6w
  • Monitor capillary glucose every hour during labour, maintain between 4-7mmol/L

Post partum:

  • STOP ALL DM drugs after birth!!! Once placenta out, no longer diabetic
  • Monitor CBG on postnatal ward and ensure no hypoglycaemia
  • Post-partum GP check up for fasting plasma glucose (6-13w) e.g. at 6w post-natal check
  • –> <6mmol/L = low probability of DM, annual testing and moderate risk of developing T2DM
  • –> 6-6.9mmol/L = high risk of T2DM
  • –> >7mmol/L = 50% chance of having T2DM and offer diagnostic test to confirm
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8
Q

What diabetic drugs are contraindicated in pregnancy?

A

Oral hypoglycaemics e.g. Gliclazide (sulphonylurea)

Liraglutide (GLP-1 agonist)

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9
Q

What is the difference between eclampsia and pre-eclampsia?

A

Eclampsia is the presence of at least 1/+ new onset seizure (tonic-clonic, 60-75s) in a women with pre-eclampsia
-> Pre-eclampsia defined as BP >140/90mmHg AFTER 20w, along with at least 1/+ of either proteinuria and/or maternal organ dysfunction (e.g. deranged renal/liver/neuro function)

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10
Q

How can you avoid pre-eclampsia?

A

Women at risk of pre-eclampsia are given 75mg OD aspirin prophylactically from 12w until birth:
-> Either 1/+ high RFs or 2/+ moderate RFs

High = previous pre-eclampsia, CKD, AI disease, T1 or T2DM, chronic hypertension (i.e. present before 20w)

Moderate = Age 40+, Primigravid, pregnancy interval of >10y, BMI of 35 or above, FHx of pre-eclampsia, multiple pregnancy

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11
Q

What is HELLP?

A

HELLP is a severe form of pre-eclampsia, standing for:

  • Haemolysis
  • Elevated liver enzymes
  • Low platelets
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12
Q

How may pre-eclampsia present in pregnant women?

A

Sx:

  • Largely asymptomatic, hence why do BP at ANC visits
  • Severe headaches
  • Visual disturbances
  • N+Vomiting
  • Epigastric/RUQ pain
  • Sudden swelling of face, feet and hands [oedema]
  • Seizures [Eclampsia]
  • Breathlessness
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13
Q

What Ix would you perform for suspected pre-eclampsia?

A

Ix:

  • Obs including blood pressure
  • Urine dipstick to check for proteinuria; if 1+ or more, then PCR quantification is done (>30mg/mmol is significant)
  • Bloods = FBC, LFTs, Coagulation screen, U&Es to assess end-organ involvement, HELLP

[DO NOT use 24h urine collection]

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14
Q

How would you manage women with pre-eclampsia? How would you treat eclampsia?

A

Mx:

  • Always give healthy lifestyle advice and urine dip at every appointment
  • Aspirin prophylaxis if RFs present/chronic HTN <20w

1st line = Labetalol 100mg BD*
2nd line = Nifedipine (e.g. if CI in asthma; note it causes tocolysis so use Methyldopa at term)
3rd line = Methyldopa 250mg BD or TDS - or IV Hydralzine may be used

Eclampsia = IV MgSO4 - potent cerebral vasodilator

NOTE: If BP is 160/110 or OVER, or 150+ with symptoms –> then they require ADMISSION and give labetalol/nifedipine and target BP of 135/85 and below
- Measured every 15-30 mins until under 160/110 and then 4x day if inpatient -> every 2d if outpatient

  • either 2 or 3x week bloods
  • ACEi and ARBs are teratogenic so B-blockers used
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15
Q

What are some important points for antenatal, intrapartum and postpartum care for women with pre-eclampsia?

A

Antenatal:

  • BP every 2d
  • FBC, LFTs and renal function either 2x/week (140/90 - 159/109mmHg) or 3x/week (160/110+ mmHg)
  • Foetal monitoring every 2w - USS, umbilical artery dopplers, CTG if abnormal results, dipstick and BP measurement

Intrapartum care:

  • Monitoring with continuous CTG
  • BP monitoring and continue antihypertensives during labour either hourly if 140/90mmHg or 15-30 mins if >160/110mmHg
  • Epidural anaesthesia should help to reduce BP
  • Antenatal CS if <34w and birth planned in next 7d
  • Consider anticonvulsants if previous eclamptic fits, birth in next 24h or features of severe pre-eclampsia

Postpartum:

  • Kept for at least 24h and discharged when
  • -> no symptoms of pre-eclampsia
  • -> BP <150/100mmHg
  • -> bloods are stable or improving
  • BP monitoring goes from 4x day as inpatient -> every other day at outpatient -> once weekly until targets achieved and antihypertensives are weaned down (130/80) and eventually stopped (~2w)
  • Refer to GP for follow up
  • Avoid diuretic treatment whilst breastfeeding as well as ARBs/ACEi apart from enalapril and captopril/Amlodipine
  • Counsel that 1 in 4/5 women will get recurrence of PET in future pregnancies, and increased risk of CVD in life
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16
Q

What are some points to mention in PACES counselling for pre-eclampsia?

A

PACES:
- Explain RFs if present and therefore requirement for prophylaxis
OR
- Explain diagnosis of pre-eclampsia = BP is higher and this can lead to complications in yourself and baby
- Epidemiology - relatively common, affects 2-8% of women
- Risks = early delivery, reduced placental function, IUGR, risks to mother e.g. seizures
- Explain treatment of labetalol +/- admission if necessary
- Explain that they will be monitored closely with regular bloods and BP measurements either 2 or 3x week
- Explain early delivery may be required/safer

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17
Q

What is obstetric cholestasis (OC) and what are the causes and associated RFs? Why is it dangerous?

A

OC = pruritic condition during pregnancy due to abnormal liver function and impaired bile flow causing bile salt deposition in the placenta and skin (in the absence of other identifiable pathology)

Cause - likely genetic and hormonal factors (i.e. membrane phospholipid defects and oestrogen impairing sulphation)

RFs = previous OC, FHx, ethnicity (South asian and south american), multiple pregnancy, pruritus on COCP
-> Affects 1% pregnancies in 2nd half of pregnancy

IT is dangerous as can lead to PPH (VitK deficiency), foetal distress, meconium delivery, PTL and IVH in baby causing intrauterine death

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18
Q

How may a woman present with OC? What investigations would you consider?

A

Sx:

  • > Pruritus with excoriations, particularly on palms and soles - worst at night
  • > Raised BR and jaundice in 20%
  • > NO rash

Ix:

  • Raised BILE ACIDS
  • Raised ALT/AST

PLUS:

  • Check baby with USS/CTG
  • Would want to do a liver screen [USS] if BA not raised/just in case to rule out there causes if unsure Coagulation screen (may be high if VitK deficient), fasting serum cholesterol (raised) and HepC serology (increased risk of OC in HepC individuals)
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19
Q

How would you manage a woman with OC?

A

Mx:

  1. Symptom relief
    - > Topical emollient and wear loose cotton clothes to help itching
    - > Sedating antihistamines e.g. chlorphenamine or promethazine
    - > Ursodeoxycholic acid - reduces itching and improves LFTs
    - > Vitamin K supplementation if clotting impaired
  2. Antenatal monitoring
    - > Weekly LFTs until delivery, checking BA level as this corresponds to delivery and Mx
    - > Twice-weekly Doppler and CTG until delivery
    - > Consultant led care
  3. Delivery -> Offer IOL at 37w
  4. Post-natal GP f/u to ensure LFTs returned to normal
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20
Q

How would you counsel a patient with OC? (PACES)

A

PACES:

  • Explain diagnosis and RFs (not entirely sure of cause, may be genetic or due to increased hormones during pregnancy but RFs are personal or FHx, multiple pregnancy etc)
  • Explain risks - stillbirth (2-3%) and premature birth and therefore need to induce labour at 37[-40]w depending on BA levels
  • Explain management - monitoring with weekly bloods and twice-weekly scans to check baby and you are well
  • Symptomatic treatment for you to reduce itching [creams, antihistamines, urso may help]
  • SAFETY NET - keep an eye on foetal movements and any reduction in them
  • High recurrence rate of 70-90% in future pregnancies
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21
Q

What is acute fatty liver of pregnancy? What are some RFs associated with it?

A

RARE pregnancy associated disorder characterised by fatty infiltration of the liver
- likely a mitochondrial disorder affecting fatty acid oxidation

RFs = nulliparity, multiple pregnancies, obesity, male foetus, pre-eclampsia

22
Q

How may women present with acute fatty liver of pregnancy? What are other DDx?

A

Sx:

  • > Normally third trimester
  • > N+V, abdominal pain/liver tenderness, jaundice, ascites, manifestations of coagulopathy (bleeding)

DDx:

  • > HELLP syndrome
  • > OC is differentiated by pruritus
23
Q

How would you Ix and manage acute fatty liver of pregnancy? What are possible complications of it?

A

Ix:

  • > Bloods - LFTs typically very elevated but ALP may also be raised due to placental production
  • > Other bloods: blood glucose (low), uric acid (high), coagulation screen
  • > USS will show fatty liver

Mx:

  • Supportive management to stabilise
  • Once stabilised, delivery is the definitive management to prevent deterioration

Complications:

  • Maternal: death (10-20%), haemorrhage (2^ to DIC), renal failure, hepatic encephalopathy, sepsis, pancreatitis
  • Foetal: death
24
Q

What are some important conditions in pregnancy, some of which are specially managed in an ObsMed clinic? What should you consider when thinking about medical conditions in pregnancy?

A 
Asthma
AI -> IBD, SLE, RhA
Thyroid disease
Cardiac disease + HTN
Epilepsy
Infections + HIV 
[Anaemia]

Effect of Pregnancy on Disease
+
Effect of Disease on Pregnancy

25
Q

How may hypothyroid disease affect a pregnancy?

A

If untreated or undertreated:

D Effects on Pregnancy:
-> Increased risk of anaemia, SGA, PET and miscarriage

P Effects on disease:

  • > T4 (Levo) can cross the placenta and therefore provide hormone to the foetus
  • > Therefore, INCREASED doses required during pregnancy (check TFTs and re-titrate for normal/low TSH), but usually 30-50% increase i.e. 25-50mcg
26
Q

Why is it important to consult women with pre-existing HTN before/during pregnancy? What must you consider in HTN-patients in the intrapartum period?

A

Many drugs used in HTN management are CI in pregnancy/have adverse effects e.g.:
-> ACEi
-> ARBs
-> Thiazides and thiazide-like diuretics
All of which cause congenital abnormalities in babies e.g. ACEi and ARBs can cause hypocalvaria (incomplete formation of skull bones) and oligohydramnios

Other medications which can be used include:

  • > Labetalol
  • > CCBs e.g. Nifedipine
  • > Alpha-blockers e.g. Doxazocin

No IM Ergometrine in HTN in intrpartum management of third stage!

27
Q

What is important to note in IBD and RhA in pregnancy?

A

IBD: [if well controlled]

  • > CD there is no increased risk of flare ups in pregnancy
  • > UC there is 2x increased risk of flare ups
  • > Monitoring for complications such as malabsorption/deficiencies and extra folic acid
  • > Aminosalycilates, Azathioprine and steroids safe in pregnancy, Inflixmab up to 20w

RhA:

  • > RhA should be well controlled for at least 3m before pregnancy
  • > Often RhA symptoms improve during pregnancy and may flare after delivery
  • > Methotrexate is contraindicated and teratogenic, causing miscarriage and congenital abnormaliteis - stopped 6M before conception
  • > Hydroxychloroquine and Sulfasalazine are safe + CS in flares
28
Q

What is classed as anaemia in pregnancy?

A 
Pregnant women with a mean Hb of: 
<110g/L in T1
<105 in T2+3
<100 post-partum
--> If <70g/L then urgent referral required

In pregnancy, plasma volume increases therefore diluting the Hb concentration

29
Q

What are the different types of anaemia you may see in pregnancy?

A

Several types of anaemia including iron-deficiency, folate-deficiency, B12 deficiency:

Iron deficiency – blood loss, inc. use, dec. absorption, dec. intake, haemolysis
–> Hypochromic microcytic anaemia, pencil cells

Folate – reduced green leafy vegetables increases neural tube defects – diet, demand, malabsorption, drugs
–> Megaloblastic anaemia (hypersegmented neutrophils, macrocytosis, thrombocytopaenia, leucopaenia)

B12 – vegans, poultry, dairy, eggs -> lack increases neural tube defects – diet, malabsorption
–> Megaloblastic anaemia (hypersegmented neutrophils, macrocytosis, thrombocytopaenia, leucopaenia)

30
Q

What are some RFs for anaemia and how may a women present?

A

RFs:

  • > Multiple pregnancy
  • > Pregnancies close together
  • > Pregnant teenager
  • > Diet!!
  • > Pre-existing anaemia
  • > Heavy vomiting in pregnancy

Sx:

  • > Fatigue
  • > Breathless, SOB
  • > Dizziness
  • > Pallor (skin, lips, nails)
  • > Tachycardia, tachypnoea
  • > B12: glossitis, depression, peripheral neuropathy, paraesthesia
  • > ALSO incidental: anaemia screened at booking + at 28w
31
Q

How would you Ix a pregnant woman with anaemia? When is it routinely screened?

A

Ix:

  • > Full exam for signs of disease or underlying cause
  • > Bloods - FBC, blood film, haematinics/iron studies (not routinely performed) and HCT
  • > NOTE: Anaemia screened at booking + at 28w

Normal MCV may indicate physiological anaemia due to increased plasma volume in pregnancy (or maybe ACD)

32
Q

How would you manage anaemia in pregnancy? What are some complications?

A

Mx:
-> Antenatally:
—> Supplements of iron/B12/folate (100-200mg TDS OD Fe) and recheck levels in 2-3w
E.g.:
- Oral ferrous sulphate (SE = constipation, black stools and abdominal pain)*
- Oral folic acid (if unknown can give with B12 as can exacerbate B12 symptoms)/5mg increased dose
- IM Hydroxycobalamin for B12
–> Increased dietary intake i..e green, leafy vegetables for all, meat and dairy for B12, nuts for folate and Fe, beans and seeds for Fe

Intrapartum:

  • > Deliver on consultant led unit
  • > IV access and G+S on admission
  • > Active Mx of third stage
  • > Consider prophylactic syntocinon
Complications:
-> Preterm or LBW
-> PP depression
-> NTD, developmental delay in child
But usually prognosis is good

*Ensure counselling for appropriate use i..e its very hard to absorb and so must take first thing in the morning on an empty stomach, no tea/coffee/milk 1h before or after, ideally with glass of orange juice (VitC)

33
Q

Why/when are i) NSAIDs ii) Opiates avoided in pregnancy? How may BB affect the foetus?

A

NSAIDs:

  • > Block prostaglandin production, which keep the PDA open and also soften the cervix and stimulate uterine contractions at delivery
  • Therefore, avoided in pregnancy unless required (e.g. RhA). Especially in T3 as can delay labour and cause premature closure of the PDA

Opiates:

  • > Use of opiates in pregnancy can cause neonatal withdrawal symptoms called NAS (neonatal abstinence syndrome)
  • > NAS presents 3-72 post-birth with irritability, tachypnoea, raised temperature and poor feeding

BB:

  • > Labetalol used for PET first line, and also cardiac conditions and migraines
  • > Effects however include FGR, hypoglycaemia and bradycardia in the neonate
34
Q

Why is asthma in pregnancy important? Complications?

A

Commonest chronic disease in pregnancy (3-12%)
Variable airway obstruction, diagnosed before pregnancy
-> Most occur between 24-36w

Usually:
-> If control before pregnancy is good, there is limited effects on pregnancy and pregnancy on asthma
-> Labour actually reduces asthma attack risk due to increased cortisol
-> All medications are safe to use in pregnancy and good control is heavily recommended!
Other:
-> RARE: FGR and brain injury if prolonged hypoxia
-> Oral CS use in T1 increases cleft lip risk
-> Preterm birth, perinatal mortality

  • Spirometry isn’t used during pregnancy for new-onset asthma unless really required
  • > Physiological changes during pregnancy occur and therefore isn’t as accurate
  • > Instead use PEF diaries
  • > PEF: moderate = 50-75%, acute-severe = 33-50%, life-threatening = <33% and near fatal is when <33% and pCO2 is raised
35
Q

How may women present with asthma in pregnancy?

A

Sx:

  • > Wheezing
  • > SOB
  • > Cough
  • > Reduced exercise tolerance
  • > Atopic Hx
  • > WORSE in mornings+//night, waking up
  • > O/E = tachypnoea, unable to complete sentences (severe), hyper inflated chest, tachycardia

Some women present first onset asthma in pregnancy around 34w

36
Q

How would you Ix and Mx a pregnant woman with asthma? What should you NOT use intrapartum?

A

Ix:

  • > Sats and Obs (HR, RR)
  • > PEF and check PEF diary
  • > ABG
  • > Bloods (FBC for infection, CRP, blood cultures, U&Es)

Mx:

  • > Regular meds continued throughout labour, bronchoconstrictors avoided
  • > Meet in obs-med clinic if severe
  • > Manage exacerbations well (take relievers as needed etc, if using salbutamol >4x a day then come back)
  • > Ensure flu vaccines taken
  • > No extra scans, screening or appointments required if well controlled
  • > Intrapartum - no extra precautions BUT do NOT use Carboprost in PPH management as can trigger asthma attacks
  • > PP - continue medications, safe in breastfeeding

Other:

  • > Acute Mx = O2, salbutamol and atrovent nebs -> Oral prednisone or IV hydrocortisone -> IV MgSO4 + senior help -> IV aminophyline -> ITU + intubation -> Discharge when PEFR > 75%, diurnal variable <25% and stable on discharge meds for 24h
  • > Chronic = SABA -> SABA + ICS -> SABA + ICS + LTRA -> LABA + ICS +/- LTRA -> increase ICS dose -> Theophyline trials or oral CS
37
Q

What things are important to consider in pregnant women with epilepsy PRE-conception? What is the risk of defects in AEDs?

A

Variable effect of pregnancy on epilepsy - most stay same or get worse (1/3) but depends on control beforehand. Risk of SUDEP

Epilepsy isn’t shown to impact the pregnancy apart from physical injury, however it is thought that due to increased stress/tiredness, it may exacerbate seizures. Risk of epilepsy in offspring also (4-5% if one parent, 15-20% if both)

Ideally women should have there epilepsy controlled with a single AED and minimal dose before getting pregnant due to all drugs having teratogenic potential and able to cross placenta*:
–> Valproate is highly teratogenic (development delay and NTD)
–> Phenytoin avoided due to clef lip and palate
–> Levetiracetam, lamotrigine (both lowest risk of congenital malformations + safest), carbamazepine (least teratogenic) are safer in pregnancy
May also need to increase med dose in pregnancy due to metabolism increase

  • AEDs all carry the 3 teratogenic risks of: congenital heart defects, NTDs and cleft lip+palate
  • -> Risk increases 2-3x from 2-3% to 4-10%
38
Q

How would you Mx epilepsy in pregnancy?

A

Mx:
1. Pre-pregnancy: counselling, increased folic acid 5mg, reduce to monotherapy if possible, explain risk of seizures getting worse and congenital malformations e.g. facial clefts, NTDs, cardiac defects (2-3x risk but still small)

  1. Antenatal: regular joint neuro-OMC check-ups, 20w anomaly scans can pick up congenital abnormalities, folic acid 5mg in T1 + VitK in last month of pregnancy, serial growth scans to assess for IUGR (every 4w from 28w)
  2. Intrapartum: Epidural recommended to reduce stressors, but delivery mode and timing is unaffected unless seizures are increasing in frequency
  3. PP: breastfeeding is safe, safety advice with baby as PP is stressful/tiring and may trigger seizures (ensure don’t bathe baby alone, change baby on the floor, don’t carry/stand alone)

Note: 1st presentation seizures in pregnancy should be treated as eclampsia until definitive diagnosis made (other causes include epilepsy, infection, SOL, CVA, OD or drug/alcohol withdrawal, metabolic disturbances)

39
Q

How would you counsel an epileptic patient?

A

PACES:

  1. Preconception = explain risks of epilepsy on pregnancy (Can get worse, effect on baby i.e. hypoxia and affect growth/brain damage). So, important to be managed well
  2. What drugs are they on - will try and get down to 1 drug and one that is safe in pregnancy. Explain risks of drugs (2-3x increased risk of congenital malformations) but these are still rare (2-3% to 4-10%) and can be detected earlier by anomaly scans. Outweighs risk of uncontrolled epilepsy
  3. Also will need to take folic acid supplements 5mg
  4. Doesn’t affect delivery mode or timing - if gets worse then need to come back as may affect it
  5. Epidural recommended to reduce stress
40
Q

Explain the management of pregnant women with HYPOthyroidism antenatally? What is a complication which may occur postnatally? What are the complications of poor management?

A

Antenatally:

  • > Thyroxine dose may need to be increased (~ 25ug at beginning of pregnancy, even if currently euthryroid)
  • > Repeat TFTs in 2w + perform in each trimester + adjust dose if required
  • > This hopes to mimic the rise seen in normal pregnancy
  • > Continue thyroid replacement therapy throughout pregnancy, aiming for biochemical euthyroidism (TSH <4mmol/L)

Postpartum [Postpartum thyroiditis]

  • > Rare (5%)
  • > Diagnosed based on 3 criteria
  • –> Patient is within or after 12m after giving birth
  • –> Clinical manifestations suggestive of hypothyroidism
  • –> TFTs alone (no need to measure TPO Abs, present in 90%)
  • > There are 3 stages - [1] thyrotoxicosis, [2] hypothyroidism and [3] euthyroid
  • > TFTs measured every 2m after thyrotoxic phase
  • > Mx with propranolol in thyrotoxic phase, and thyroxine in hypothyroid phase

Sub-optimal Mx is associated with pregnancy loss and developmental delay

41
Q

Explain the management of pregnant women with HYPERthyroidism? What are the side effects of these drugs and uncontrolled hyperthyroidism in pregnancy?

A

Mx:

  • > Treated medically at lowest acceptable dose, not surgically, with PTU (T1) or Carbimazole (T2+3)
  • > 33% women can actually stop treatment in pregnancy but doses require adjustment postpartum to prevent relapse
  • > Radioactive iodine contraindicated as obliterates the foetal thyroid
  • > Women with TSH-receptor Abs should have neonate review as these Abs can cross placenta

SEs:

  • Foetal hypothyroidism from high-doses crossing the placenta
  • Agranulocytosis (regular checks of maternal WCC)

Uncontrolled SEs:
- Miscarriage, PTL, IUGR

42
Q

How would you manage hypo and hyperparathyroidism in pregnancy? What are the risks of it?

A

Hypoparathyroidism:

  • Increased risk of T2 miscarriage
  • Neonatal rickets + foetal hypocalcaemia
  • Mx = VitD, oral calcium supplements and regular monitoring of Ca and albumin

Hyperparathyroidism:

  • If severe, surgery may be indicated
  • Mild disease can be Mx = adequate hydration and low calcium diet
  • Risks of miscarriage, PTL, IU death and neonatal tetany
43
Q

What physiologically occurs to thyroid hormone levels in pregnancy? When are TFTs done in pregnancy?

A

Normally, in the 1st trimester, a fall in TSH and rise in T4 is expected –> free T4 then falls with advancing gestation

Booking visit screening = TFTs done in:

  • > Current thyroid disease
  • > Previous thyroid disease
  • > 1st degree FHx of thyroid disease
  • > AI conditions e.g Coeliacs, T1/2DM, GDM
44
Q

Name 5 skin diseases/conditions seen in pregnancy?

A
  • > Pemphigoid gestationis
  • > Polymorphic eruption of pregnancy (PUPPP - pruritic urticarial papules and plaques of pregnancy)
  • > Prurigo of pregnancy
  • > Pruritus folliculitis
  • > Atopic eczema
45
Q

What are some physiological skin changes seen in pregnancy?

A
  • > Pre-existing conditions like acne may flare up, requiring antibiotics e.g. erythromycin [no retinoids]
  • > Increased pigmentation (face, areola, linea nigra)
  • > Spider naevi
  • > Hand and nipple eczema common postpartum
  • > Psoriasis - topical steroids
46
Q

How does pemphigoid gestationis present? How is it managed?

A

PG - rare, pruritic AI bullous disorder

  • > Presents in late 2nd/3rd trimester
  • > Lesions start on abdomen usually [around umbilicus] –> widespread clustered blisters which spare the face
  • > Mx = potent topical steroids or oral prednisone to relieve pruritus and stop new blister formation
47
Q

How does PEP/PUPPP present? How is it managed?

A

PEP - self limiting pruritic inflammatory disorder

  • > Rash which SPARES the umbilicus
  • > Presents in 3rd trimester or immediately postpartum
  • > Begins in lower abdomen, including pregnancy striae, then may extend to thick, buttocks, legs, arms [spares umbilicus, rarely face/hands/feet]
  • > Mx = symptomatic treatment, associated with preterm and SGA deliveries but no increase in pregnancy loss, recurs in most pregnancies
48
Q

How does prurigo of pregnancy present? How is it managed?

A

Common pruritic disorder

  • > Affects 20% normal pregnancy
  • > Do LFTs to exclude OC
  • > Starts 3rd trimester (25-30w), resolves after delivery, no effect on mother or baby
  • > Present with excoriated papule on extensor limbs, abdomen and shoulder
  • > Mx = symptomatic, topical steroids and emollients
49
Q

How does pruritic folliculitis present? How is it managed?

A

Pruritic follicular eruption with papules and pustules affecting trunk and can involve limbs

  • > 2/3rd trimester, resolve a week after delivery
  • > Acne - hormone-induced type
  • > Mx = topical steroids
50
Q

How does atopic eczema in pregnancy present? How is it managed?

A

Commonest pregnancy rash, affects 5% population

Mx = emollients and bath additives, potentially steroids

51
Q

What are some key points to remember regarding cardiac conditions in pregnancy? What is peripartum cardiomyopathy?

A

Includes pre-existing cardiac conditions but also peripartum cardiomyopathy

  • –> which is new onset CM and HF within the last month of pregnancy to 5m postpartum
  • -> Physiologically, pregnancy means an increased CO and women with cardiac disease are not able to increase the CO leading to uterine hypo perfusion and pulmonary oedema [Pregnancy -> Disease]
  • -> Class by NYHA

Disease -> pregnancy
= Recurrence, maternal cyanosis and foetal hypoxia, FGR, effects of maternal drugs (FGR, foetal loss, teratogenicity)

Antenatal:

  • > ECHO at booking and at 28w
  • > Anticoagulation (LMWH) for patients with congenital heart disease who have PH or artificial valves/risk of AF

Intrapartum

  • > Most cases, aim to wait for spontaneous labour [induction may be used in v high-risk women so enough/suitable people available]
  • > 2nd stage labour is kept short with elective forceps/ventouse to reduce maternal effort/need for increased CO
  • > NO ergometrine so use syntocinon ONLY for 3rd stage
  • > Epidural recommended for pain-related stress
  • > Prophylactic antibiotics for those with structural heart defects (endocarditis)
  • > Avoid supine position

O&G (7 decks)

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