Pregnancy Flashcards
Key antenatal care appointments
Booking - 10wks or under
Dating - 12wks
Anomaly - 20wks
Purpose of booking scan (10wks or under)
Sickle cell, thalassemia before 10wks
Folate supplementation
Nutrition
Smoking, alcohol
Purpose of dating scan (12wks)
US for birthday, number
- combined blood test for Downs, Edwards, Patau
- nuchal translucency scan
May do blood test for
-syphyllis, HepB, HIV, Rubella
Purpose of anomaly scan (20wks)
US scan for 11 congenital issues
- anencephaly
- open spina bifida
- cleft lip
Describe the combined test for Downs, Edwards and Pataus
12wks
PAPPA, bhCG, nuchal translucency + maternal age
-Downs - low PAPPA, high bhCG, high NT
How would you use CRL?
-important landmarks
How would you use fundal height?
Most accurate estimation of gestational age in early pregnancy between 6-13wks
After 13wks => head circumference, biparietal, femur length
Cardiac activity present with CRL > 7mm
Fundal height in cm corresponds to gestational age in wks between 24-36wks
When would amniocentesis/CVS/NIPT be offered?
Screening suggests Downs, Edwards, Pataus
Past pregnancy affected
FHx
Amniotic fluid removed
-genetic analysis of fetal cells
Chorionic villus sampling
-genetic analysis of placental cells
Both have a 1% risk of miscarriage
NIPT
-fetal DNA found in maternal blood for chromosomal abnormalities
Supplements
- dosage
- reasoning
Folate
Preconception - 400mcg
PC+obesity - 5mg
Reduce NTD incidence by wk12
*FHx/PMH
*diabetic
*obese
*on antiepileptic meds
VitD
Pregnant -10ug
-Fetal skeleton accumulates Ca from maternal stored
-requires vitamin D from sun and diet (fish, egg, meat)
VTE prophylaxis?
35+
BMI 30+
Smoker
Parity 3+
Multigravid
Current PET
Past VTE
IVF
Gross varicose veins
Immobility
FHx of unprovoked VTE
Low risk thrombophilia
3 = heparin from 28wks - 6wk postnatal
4+ = heparin now - 6wk postnatal
DVT before delivery = continue heparin for 3months
Cervical cancer screening
Sample tested for high risk strains of HPV
- if positive => cytological examination
- if positive => colposcopy
25-49 = every 3 years
50-64 = every 5 years
Resp changes in pregnancy
- ventilation
- RR
- TV
- PO2, PCO2
- pH, HCO3-
- diaphragm, ribcage
Ventilation increases
RR no change
TV increases (P on resp center)
PO2 increases
Overbreathing => PCO2 fall, remove extra fetal CO2
HCO3 decreases (increased CO2 buffering)
pH resp alk compensation possible
Diaphragm moves up as uterus moves up
Ribcage moves up and expands to the side
CV changes
- HR
- CO
- SV
- systolic, diastolic BP
Haemodynamic changes
- BV
- RBC, haematocrit, O2 loading
- platelet and coagulation
- WBC
- [lipid]
- [water]
HR increases
CO increases
SV increases
systolic BP no change
diastolic BP falls (P VD)
BV increases
RBC increases, haematocrit falls due to haemodilution
O2 loading increases (higher DPG)
Platelets decrease
Coagulation increases, fibrinolytic decreases
WBC increases
[lipid soluble molecules] increases, especially TAGs for growth
[water soluble molecules] deacreases due to haemodilution
-folate actively used
Regional flow of blood
- uterus, kidney, skin
- skin
- other
Uterus, renal increases
Skin increases in extremities => increased nail, hair growth, nosebleeds, stuffiness, no Raynauds
Other
-decreases
How does the renal system change
- GFR
- Na, water uptake
- [urea, creatinine]
- urinary retention
GFR increases, excrete fetal waste
Na, water uptake increased
-maintain PV
[urea, creatinine] decreased due to increased GFR
Urinary retention increases (P SM relax)
Urinary frequency increases
-GFR increases and uterus pushes on bladder
GI system
- sphincter tone
- motility
Sphincter tone decreases
-reflux
Motility decreases
-constipation, increased nutrient uptake
Oestrogen
- source
- function
Ovaries, placenta, blood
- myometrial growth
- breast growth
Progesterone
- source
- function
Syncytiotrophoblast produces bhCG => corpus luteum produces P
Placenta starts production at 6 weeks, takes over at 12 weeks
Inhibits uterine contractions by
1. Inhibiting prostaglandin production
2. Decreasing sensitivity to oxytocin, allows for development of lobules and alveoli
hCG
- source
- function
hPL
- source
- function
Leptin
-function
Placental growth factor
-function
Syncytiotrophoblast => maintain CL until wk7
Stimulate TSH receptors => increase thyroid activity
Syncytiotrophoblast
Maternal lipolysis, diabetogenic => increase FFA, glucose for fetus
Stimulate AA, FA transport in placental
Aid placental survival
Angiogenesis
Prolactin
Increases in pregnancy due to O increase
- initiates, maintains milk secretion
- needed for expression of mammotropic effects of O, P
- O, P directly antagonse effects of PRL on milk synthesis
What is a normal birth
- epidemiology of normal birth
- benefits of normal birth
37-42wks, spontaneous labour and delivery
Proportion of natural births decrease with age
- avoid surgical risks
- colonisation of baby
- increase success breastfeeding
- increased bonding
Changes leading up to labour
Uterine contractions increase in frequency for several nights prior
+ve feedback loop
increased OXY => increased PG synth
Fetal CRH => ACTH causes
1. DHEA, DHEAS =(aromatase)=> increased O
2. Cortisol => lung maturation, surfactant prod, increased placental PG
Fetal movement => maternal OXY increase
Placenta => CRH, OXY prod
1st stage of labour
- latent
- active
Latent (can last for days, on and off)
- painful contractions
- some cervical effacement, dilation
Active - 4cm onwards
-regular painful contractions
Transitional stage of labour
10cm dilated
More frequent contractions
Mood changes, sweating
Greater urge to push
2nd stage of labour
- latent
- active
Passive
- frequency falls but v strong contractions
- no urges
Active
- expulsive contractions
- delivery of head, ant, post shoulder, lower body
3rd stage of labour
Placental separation => expulsion of membrane, uterine contraction
Active management
- OXY given
- cord clamped and cut 5mins after birth
- cord pulled out after placental separation
Physiological management
- no routine drugs
- clamped when pulsation stops
- maternal delivery
Benefits of immediate skin to skin contact
- mother
- child
Maternal
- successful breastfeeding
- latching
- feed longer and exclusively
Fetal
- maintain temp, HR, RR, BP, glucose
- less likely to cry
Pain relief that can be used
- not drugs
- drugs
Non drug
- breathe, relax
- massage
- water
Drugs
- entonox (gas and air)
- opioids (diamorph)
- epidural
Preeclampsia risk factors
24wks onwards
- past PET, FHx PET
- multigravid, nulliparous
- chronic HTN, high BMI, DM
- high maternal age
- APS
Placental hypoperfusion due to defective spiral artery remodelling => pro inflammatory cytokines
Systemic VC, endothelial dysfunction => HTN, end organ damage
Leads to HELLP (hemolysis, elevated liver enzymes, low platelets)
Preeclampsia signs and symptoms in
-mother
-baby
Mother
HTN => blurry vision, severe headaches
Proteinuria on dipstick
Peripheral edema => weight gain
N+V, abdo pain
May lead to
- seizures
- HTN, elevated liver enzymes, low platelets
- stroke
Unborn
-IUGR
Management
- at risk, symptomatic
- chronic HTN
- proteinuria, no HTN
Prevention - 75mg of aspirin from 12wks onwards
If they have symptoms => hospital
Lifestyle changes to manage BP => target 135
Stop ACEi, ARB => increased risk of AE on baby in 2nd, 3rd trimester
Stop thiazides
Specialist support for alternatives
-1st line labetolol (alt, nifedipine, methyldopa)
Preeclampsia is still a possibility, proteinuria 2+ => specialist assessment even if no other symptoms, UTI likely
-UTI, if leukocytes nitrites +ve, proteinuria 1+ => MSU, follow up in a week
Describe the structure of the placenta and how substances are moved between the mother and the fetus
Maternal spiral arteries and veins
-substances diffuse from the villi basal plate =(intervillous space)=> chorionic villi
1 umbilical vein => fetus => 2 umbilical arteries
Blood does not mix
Describe the structure of the early spiral arteries
Initally histitrophic
-spiral arteries blocked by trophoblastic plug
Becomes haemotrophic
-plug removed, mouth expands to accommodate more blood
Describe how
- CO2
- Glucose
- FA
- AA is trasnported
CO2
-diffuses across syncytiotrophoblast, CA buffered
Glucose
-GLUT1 across STB
FA
- LPL breaks down TAG in LP => FA
- transported to FATP bound to FABP
AA
- NaAAcotransport, nonessential, essential AA exchange
- Na, Cl cotranport
How is fluid homeostasis maintained in the fetus
Maintained by placenta, fetal membrane
- kidneys provide dilute urine (immature ADH)
- bladder fills and empties every 20-30mins
What is found in the amniotic fluid
Urine
Amniotic membrane secretions
Fetal lung secretions
Saliva
Fetal and amniotic cells
Fetus swallows fluid from wk12 onwards
How doe the GI system develop in the fetus
-digestive enzymes, when are they found from
-digestive hormones, where and when are they found from
When is it formed by
Formed by wk19
Digestive enzymes
-present by wk9, mature at term
Gastrin motilin, somatostatin
- regulate growth and dev
- gut synthesised, mature by wk24
Describe how glucose homeostasis is maintained
- where does glucose come from
- how is it used
- where does the insulin come from
Dependent on placental transfer
- glycogen storage in fetal liver
- not capable of gluconeogenesis
Fetal insulin and IGF
- lipogenesis
- anabolic, anticatabolic effects for growth
Describe the physiological control of the fetal heart
HR affected by ANS control (PNS dominated)
- NA/A
- chemo/baroceptors
Describe the circulatory route of blood from the placenta
Describe the fetal haemoglobin and its characteristics
Placenta => 1 umbilical vein => ductus venosus (bypass liver) => foramen ovale (bypass pulmonary circulatotion) => ductus arteriosus (bypass lungs) => 2 umbilical arteries
HbF
- increased O2 affinity, [HbF]
- decreased PO2
HbA
-increases from wk28
Describe the fetal hypoxic response
Decreased HR
Decreased cerebral resistance
Increased umbilical artery resistance
Increased flow to heart, adrenals
Decreased flow to kidneys => oligohydramnios
Describe the cells in the lungs and their functions
T2 alveolar cells secrete surfactant from wk24 => decrease alveolar surface tension
-PL, C, protein
T1 alveolar cells
What is neonatal resp distress
What is the pathophysiology
How would you manage this
Not enough surfactant
Decreased compliance, alveolar collapse
Increased work to breathe
Exogenous surfactant
-synthetic/modified natural
Cortisol
-stimulate lung dev and surfactant prod
How does
-umbilical clamping
-inspiration
-secretions
change at delivery
Umbilical clamping
-decreased RA pressure, FO closes
Inspiration
- VD of pulmonary arteries => decreased R
- decreased F via FO, DA
Secretions
- lung secretions decrease
- surfactant increases
How is placental transfer used in the production of fetal and maternal hormones
Maternal cholesterol
Converted to pregnenolone
-fetus converts this into DHA, DHAS
-can be converted into types of estrogen for maternal use
What are the 3 stages of embryo growth
Stage 1 (4-20wk)
-hyperplasia, rapid mitosis, increase in DNA
Stage 2 (21-28)
- hyperplasia and hypertrophy
- declining mitosis but cell size increases
- greatest weight gain here
Stage 3 (29-40)
- hypertrophy
- rapid increase in cell size
- accumulate fat, muscle, connective tissue
- greatest variation in weight here
What is appropriate for gestational age
Following the expected trends in weight as gestational age increases
What is fetal growth restriction
- what are the short term consequences
- what are the long term consequences
Growth doesn’t follow expected trend
Pathological restriction/IUGR
-stillbirth
-seizures
-ICU admission
-hypothermia, hypoglycaemia
Long term impact
- CHD, HT
- T2D, strokes
What does it mean to be small for gestational age
- what are the 2 main types
- management
<3-10th cent
Following trends in weight but below estimations consistently
Symmetrical SGA - prolonged poor growth from early pregnancy
- healthy, normal
- chromosomal, congenital issues
- alcohol, cigarettes, drugs
- TORCHZS
- malnutrition
Assess for pathological cause, infections
Monitor growth frequently
Asymmetrical - placenta fails to provide adequate nutrition late in pregnancy
- placental insufficiency, PET
- alcohol, cigarettes, drugs
- congenital, chromosomal
Assess for absent end diastolic flow in umbilical circulation with Doppler
Monitor growth frequently
Consider early delivery
How would you detect, prevent and manage SGA
Detection and prevention
- decreased PAPPA, high uterine flow resistance (poor placental function)
- aspirin, monitor growth, decrease PET risk
Management
- if FGR=> early delivery with steroids
- if SGA=> induce before term
How would you interpret a fetal doppler for the
- umbilical artery
- MCA
Fetal doppler, judge direction and quality of blood flow
-generates pulsatility index
Umbilical artery
- if line falls under x axis => flow reversed
- if line falls on x axis => no flow at that point
- if pulsatility index increases, blood has to work harder to be moved around
MCA
- if diastole is higher than expected => MCA being prioritised for some reason
- if PI decreases => be worried
What are the possible growth outcomes for twins
- what birth would be low risk
- what births would be high risk
Both grow normally
Both SGA
AGA, FGR => may need to deliver at different times
Low risk
-DC
High risk
- MC
- potential selective IUGR
- potential twin to twin transfusion
What does it mean to be large for gestational age
-what are the causes
-what are the risks
How would you manage this
> 90th centile
Healthy large => large parents
Poorly controlled maternal diabetes
- shoulder dystocia (fat accumulates on shoulders)
- hypoglycaemia (exposed to increased glucose, produces extra insulin
- increased chance of maternal complications
- PPH
- Caesarean may be needed
What are the consequences of shoulder dystocia
Brachial plexus injury
-Erbs palsy
Fractured humerus, clavicle
-Asphyxia, death
What is the puerperium
What happens to the
-uterus
-perineum
-breast
-abdomen
-blood
-MH
What can go wrong
6-8wks, return to non pregnant state
Uterus
- involution (PPH if atonic)
- lochia (infection, discharge not sterile)
Perineum
-healing from episiotomy, stretch (pain, dyspareunia, infection
Breast
-lactation (pain, infesction, mastitis)
Abdomen
- healing from CS, stretch (pain, infection)
- weakened pelvic floor (SM still realxed) => urinary incontinence, retention, constipation
Blood
- decreased BV (anaemia if PPH)
- immunity and clotting returns to normal (infection, sepsis, thrombosis)
MH
- adjusting
- anxiety, fatigue, baby blues (PN depression, PTSD, puerperial psychoses)
What are the signs and symptoms of puerperal sepsis
Fever
Diarhhoea, vomit
Breast redness
Abdo/pelvic pain
Wound infection, foul discharge
Urinary symptoms
Delay on involution
Heavy lochia
What are the signs and symptoms of PET
HTN
Headaches
Proteinuria
Edema
Visual changes
What are the signs and symptoms of PN depression
What are the signs and symptoms of PNPTDS
What are the signs and symptoms of puerperal psychosis
How would you manage this
Common with depression
Problems bonding
Common with PTSD
Common with psychoses
Self harm and baby
Self help
Therapy
Meds
What is the leading cause of maternal death during this period
Thrombosis
Describe the route of milk
Lobule => duct => ampule that holds milk => nipple
Grows in pregnancy => increase in milk producing cells
Describe the onset of lactation
- antenatally
- postnatally
Antenatal
- PRL secretion increases during pregnancy
- no response as P and O is high, stops actions
Postnatal
- PRL decreases but steady prod maintained
- suckling increases PRL => increased milk
What is colostrum
-why is this important
What is the main component of breast milk
1st milk
gold thick conc milk
-immunoglobulin rich
Lipid and sugar rich
How is milk production stimulated
Suckling => positive feedback
Hypothalamic VIP production stimulated => increased PRL, decreased D
Strength of suck determines amount of PRL produced, vol of milk produced
How is milk ejected
Suckling => OXY release
Myoepithelial cells contract around lobule
Milk ejected out of nipple
Can be conditioned by crying
Hypertensive medications that are
- to be avoided
- safe alternatives
To be avoided
- ACEi, ARB
- diuretics
- most Bb
Safe alternatives
- 1st line = labetolol
- 2nd line = nifedipine
- 3rd line = methyldopa
NSAIDs that are
- to be avoided
- safe alternatives
To be avoided
- high doseaspirin
- ibuprofen, other NSAIDs
Use paracetamol instead
Anticoagulants that are
- to be avoided
- safe alternatives
To be avoided
- warfarin
- DOACs
Safe alternatives
-heparin
