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Endocrinology, O&G, Paediatric Core Conditions > Pregnancy > Flashcards

Pregnancy Flashcards

1
Q

Key antenatal care appointments

A

Booking - 10wks or under
Dating - 12wks
Anomaly - 20wks

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2
Q

Purpose of booking scan (10wks or under)

A

Sickle cell, thalassemia before 10wks

Folate supplementation
Nutrition
Smoking, alcohol

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3
Q

Purpose of dating scan (12wks)

A

US for birthday, number

  • combined blood test for Downs, Edwards, Patau
  • nuchal translucency scan

May do blood test for
-syphyllis, HepB, HIV, Rubella

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4
Q

Purpose of anomaly scan (20wks)

A

US scan for 11 congenital issues

  • anencephaly
  • open spina bifida
  • cleft lip
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5
Q

Describe the combined test for Downs, Edwards and Pataus

A

12wks
PAPPA, bhCG, nuchal translucency + maternal age
-Downs - low PAPPA, high bhCG, high NT

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6
Q

How would you use CRL?
-important landmarks
How would you use fundal height?

A

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

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7
Q

When would amniocentesis/CVS/NIPT be offered?

A

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

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8
Q

Supplements

  • dosage
  • reasoning
A

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)

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9
Q

VTE prophylaxis?

A

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

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10
Q

Cervical cancer screening

A

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

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11
Q

Resp changes in pregnancy
- ventilation
- RR
- TV
- PO2, PCO2
- pH, HCO3-
- diaphragm, ribcage

A

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

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12
Q

CV changes

  • HR
  • CO
  • SV
  • systolic, diastolic BP

Haemodynamic changes

  • BV
  • RBC, haematocrit, O2 loading
  • platelet and coagulation
  • WBC
  • [lipid]
  • [water]
A

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

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13
Q

Regional flow of blood

  • uterus, kidney, skin
  • skin
  • other
A

Uterus, renal increases

Skin increases in extremities => increased nail, hair growth, nosebleeds, stuffiness, no Raynauds

Other
-decreases

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14
Q

How does the renal system change

  • GFR
  • Na, water uptake
  • [urea, creatinine]
  • urinary retention
A

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

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15
Q

GI system

  • sphincter tone
  • motility
A

Sphincter tone decreases
-reflux
Motility decreases
-constipation, increased nutrient uptake

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16
Q

Oestrogen

  • source
  • function
A

Ovaries, placenta, blood

  • myometrial growth
  • breast growth
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17
Q

Progesterone

  • source
  • function
A

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

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18
Q

hCG
- source
- function

hPL
- source
- function

Leptin
-function

Placental growth factor
-function

A

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

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19
Q

Prolactin

A

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
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20
Q

What is a normal birth

  • epidemiology of normal birth
  • benefits of normal birth
A

37-42wks, spontaneous labour and delivery

Proportion of natural births decrease with age

  • avoid surgical risks
  • colonisation of baby
  • increase success breastfeeding
  • increased bonding
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21
Q

Changes leading up to labour

A

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

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22
Q

1st stage of labour

  • latent
  • active
A

Latent (can last for days, on and off)

  • painful contractions
  • some cervical effacement, dilation

Active - 4cm onwards
-regular painful contractions

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23
Q

Transitional stage of labour

A

10cm dilated
More frequent contractions
Mood changes, sweating
Greater urge to push

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24
Q

2nd stage of labour

  • latent
  • active
A

Passive

  • frequency falls but v strong contractions
  • no urges

Active

  • expulsive contractions
  • delivery of head, ant, post shoulder, lower body
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25
Q

3rd stage of labour

A

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
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26
Q

Benefits of immediate skin to skin contact

  • mother
  • child
A

Maternal

  • successful breastfeeding
    • latching
    • feed longer and exclusively

Fetal

  • maintain temp, HR, RR, BP, glucose
  • less likely to cry
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27
Q

Pain relief that can be used

  • not drugs
  • drugs
A

Non drug

  • breathe, relax
  • massage
  • water

Drugs

  • entonox (gas and air)
  • opioids (diamorph)
  • epidural
28
Q

Preeclampsia risk factors

A

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)

29
Q

Preeclampsia signs and symptoms in
-mother
-baby

A

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

30
Q

Management

  • at risk, symptomatic
  • chronic HTN
  • proteinuria, no HTN
A

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

31
Q

Describe the structure of the placenta and how substances are moved between the mother and the fetus

A

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

32
Q

Describe the structure of the early spiral arteries

A

Initally histitrophic
-spiral arteries blocked by trophoblastic plug

Becomes haemotrophic
-plug removed, mouth expands to accommodate more blood

33
Q

Describe how

  • CO2
  • Glucose
  • FA
  • AA is trasnported
A

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

34
Q

How is fluid homeostasis maintained in the fetus

A

Maintained by placenta, fetal membrane

  • kidneys provide dilute urine (immature ADH)
  • bladder fills and empties every 20-30mins
35
Q

What is found in the amniotic fluid

A

Urine
Amniotic membrane secretions
Fetal lung secretions
Saliva
Fetal and amniotic cells

Fetus swallows fluid from wk12 onwards

36
Q

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

A

Formed by wk19

Digestive enzymes
-present by wk9, mature at term

Gastrin motilin, somatostatin

  • regulate growth and dev
  • gut synthesised, mature by wk24
37
Q

Describe how glucose homeostasis is maintained

  • where does glucose come from
  • how is it used
  • where does the insulin come from
A

Dependent on placental transfer

  • glycogen storage in fetal liver
  • not capable of gluconeogenesis

Fetal insulin and IGF

  • lipogenesis
  • anabolic, anticatabolic effects for growth
38
Q

Describe the physiological control of the fetal heart

A

HR affected by ANS control (PNS dominated)

  • NA/A
  • chemo/baroceptors
39
Q

Describe the circulatory route of blood from the placenta

Describe the fetal haemoglobin and its characteristics

A

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

40
Q

Describe the fetal hypoxic response

A

Decreased HR
Decreased cerebral resistance
Increased umbilical artery resistance
Increased flow to heart, adrenals
Decreased flow to kidneys => oligohydramnios

41
Q

Describe the cells in the lungs and their functions

A

T2 alveolar cells secrete surfactant from wk24 => decrease alveolar surface tension
-PL, C, protein

T1 alveolar cells

42
Q

What is neonatal resp distress
What is the pathophysiology
How would you manage this

A

Not enough surfactant

Decreased compliance, alveolar collapse
Increased work to breathe

Exogenous surfactant
-synthetic/modified natural
Cortisol
-stimulate lung dev and surfactant prod

43
Q

How does
-umbilical clamping
-inspiration
-secretions
change at delivery

A

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
44
Q

How is placental transfer used in the production of fetal and maternal hormones

A

Maternal cholesterol
Converted to pregnenolone
-fetus converts this into DHA, DHAS
-can be converted into types of estrogen for maternal use

45
Q

What are the 3 stages of embryo growth

A

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
46
Q

What is appropriate for gestational age

A

Following the expected trends in weight as gestational age increases

47
Q

What is fetal growth restriction

  • what are the short term consequences
  • what are the long term consequences
A

Growth doesn’t follow expected trend
Pathological restriction/IUGR
-stillbirth
-seizures
-ICU admission
-hypothermia, hypoglycaemia

Long term impact
- CHD, HT
- T2D, strokes

48
Q

What does it mean to be small for gestational age

  • what are the 2 main types
  • management
A

<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

49
Q

How would you detect, prevent and manage SGA

A

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
50
Q

How would you interpret a fetal doppler for the

  • umbilical artery
  • MCA
A

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
51
Q

What are the possible growth outcomes for twins

  • what birth would be low risk
  • what births would be high risk
A

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
52
Q

What does it mean to be large for gestational age
-what are the causes
-what are the risks
How would you manage this

A

> 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
53
Q

What are the consequences of shoulder dystocia

A

Brachial plexus injury
-Erbs palsy

Fractured humerus, clavicle
-Asphyxia, death

54
Q

What is the puerperium
What happens to the
-uterus
-perineum
-breast
-abdomen
-blood
-MH

What can go wrong

A

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)

55
Q

What are the signs and symptoms of puerperal sepsis

A

Fever
Diarhhoea, vomit
Breast redness
Abdo/pelvic pain
Wound infection, foul discharge
Urinary symptoms
Delay on involution
Heavy lochia

56
Q

What are the signs and symptoms of PET

A

HTN
Headaches
Proteinuria
Edema
Visual changes

57
Q

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

A

Common with depression
Problems bonding

Common with PTSD

Common with psychoses
Self harm and baby

Self help
Therapy
Meds

58
Q

What is the leading cause of maternal death during this period

A

Thrombosis

59
Q

Describe the route of milk

A

Lobule => duct => ampule that holds milk => nipple

Grows in pregnancy => increase in milk producing cells

60
Q

Describe the onset of lactation

  • antenatally
  • postnatally
A

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
61
Q

What is colostrum
-why is this important

What is the main component of breast milk

A

1st milk
gold thick conc milk
-immunoglobulin rich

Lipid and sugar rich

62
Q

How is milk production stimulated

A

Suckling => positive feedback
Hypothalamic VIP production stimulated => increased PRL, decreased D

Strength of suck determines amount of PRL produced, vol of milk produced

63
Q

How is milk ejected

A

Suckling => OXY release
Myoepithelial cells contract around lobule
Milk ejected out of nipple

Can be conditioned by crying

64
Q

Hypertensive medications that are

  • to be avoided
  • safe alternatives
A

To be avoided

  • ACEi, ARB
  • diuretics
  • most Bb

Safe alternatives

  • 1st line = labetolol
  • 2nd line = nifedipine
  • 3rd line = methyldopa
65
Q

NSAIDs that are

  • to be avoided
  • safe alternatives
A

To be avoided
- high doseaspirin
- ibuprofen, other NSAIDs

Use paracetamol instead

66
Q

Anticoagulants that are

  • to be avoided
  • safe alternatives
A

To be avoided

  • warfarin
  • DOACs

Safe alternatives
-heparin

Endocrinology, O&G, Paediatric Core Conditions (64 decks)

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