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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
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
26
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
27
Pain relief that can be used - not drugs - drugs
Non drug - breathe, relax - massage - water Drugs - entonox (gas and air) - opioids (diamorph) - epidural
28
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)
29
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
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
Describe the physiological control of the fetal heart
HR affected by ANS control (PNS dominated) - NA/A - chemo/baroceptors
39
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
40
Describe the fetal hypoxic response
Decreased HR Decreased cerebral resistance Increased umbilical artery resistance Increased flow to heart, adrenals Decreased flow to kidneys => oligohydramnios
41
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
42
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
43
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
44
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
45
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
46
What is appropriate for gestational age
Following the expected trends in weight as gestational age increases
47
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
48
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
49
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
50
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
51
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
52
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
53
What are the consequences of shoulder dystocia
Brachial plexus injury -Erbs palsy Fractured humerus, clavicle -Asphyxia, death
54
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)
55
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
56
What are the signs and symptoms of PET
HTN Headaches Proteinuria Edema Visual changes
57
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
58
What is the leading cause of maternal death during this period
Thrombosis
59
Describe the route of milk
Lobule => duct => ampule that holds milk => nipple Grows in pregnancy => increase in milk producing cells
60
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
61
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
62
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
63
How is milk ejected
Suckling => OXY release Myoepithelial cells contract around lobule Milk ejected out of nipple Can be conditioned by crying
64
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
65
NSAIDs that are - to be avoided - safe alternatives
To be avoided - high doseaspirin - ibuprofen, other NSAIDs Use paracetamol instead
66
Anticoagulants that are - to be avoided - safe alternatives
To be avoided - warfarin - DOACs Safe alternatives -heparin

Endocrinology, O&G, Paediatric Core Conditions (65 decks)

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