pregnancy Flashcards

1
Q

describe the trimesters

A

0-13 weeks: spontaneous loss of pregnany common here
14-26 weeks: end of this trimester marks limit of infant survival
27-39 weeks

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2
Q

what is term?

A

39-40 weeks

around 280 days (40 weeks) since LMP

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3
Q

what are the main maternal changes?

A
  • abdo changes seen from 2nd trimester
  • inc. weight
  • inc. blood clotting
  • inc. vaginal mucous
  • altered appetite
  • altered joints
  • inc. hormone levels
  • dec. BP
  • morning sickness
  • altered emotion, brain function
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4
Q

when is the start of the pregnancy?

A
  • from first day of last menstrual period

- embryologists and an obstetrician use different time scales

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5
Q

describe the IVF pregnancy timing

A
  • fertilisation occurs 2-3 days before

- difference in time of 2/2.5 weeks from GA and GA in IVF pregnancy

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6
Q

what causes the inc. weight in mothers? how much?

A
  • 10-15kg

- baby, placenta, amniotic fluid, inc. fluid retention, inc. stores

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7
Q

what hormones are inc.in mothers?

A
  • hCG: peaks 1st trimester, dec. thereafter

- progesterone, oestrogens, lactogen: slowly inc. as pregnancy progresses

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8
Q

why is progesterone important?

A
  • key to maintaining pregnancy

- progesterone antagonists = loss of pregnancy at all gestational stages

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9
Q

what is the source of progesterone?

A
  • fertilisation –> 8 weeks: corpus luteum source via hCG
    8+ weeks: placenta supplies progesterone
    change over = luteo-placental shift
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10
Q

describe the oestrogen source

A
  • fertilisation –> luteo-placental shift = corpus luteum

- 8+ weeks = complex interplay b/ foetal/maternal adrenals and placenta

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11
Q

describe this complex interplay

A
  • human placenta doesn’t express enzymes needed to convert pregnenolone to androgens
  • this occurs in foetal adrenals
  • weak androgen produced (DHEA) sulphated to give DHEA-S
  • DHEA-S is inactive so female foetus not exposed to androgens
  • DHEA-S goes to placenta to be converted to 17-beta oestradiol
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12
Q

why are there low FSH and LH levels throughout?

A

high steroid levels suppress HPG-axis

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13
Q

why is there an inc. blood clotting tendency?

A
  • protective against losing blood at delivery
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14
Q

when is blood pressure lowest?

A
  • during 2nd trimester

- why pregnancy women should not stand for too long

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15
Q

why is there an inc. basal body temp?

A
  • possible by progesterone

- mediated by foetal size

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16
Q

what causes the altered brain function?

A

high levels of steroid e.g. progesterone

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17
Q

what causes the altered appetite?

A
  • due to height of fundus
  • stomach may be impinged
  • mother may need smaller meals
18
Q

why is there altered flui balance and frequent urination?

A
  • kidney functions change –> around 50% inc in plasma fluid volume by term
  • inc, abdo size puts pressure on ballder
19
Q

why are there altered joints?

A
  • changes in pelvis to make connections more flexible to permit childbirth
20
Q

why is there an altered immune system?

A
  • production of factors: suppress maternal immune system from utero-placental interface
    results in reduction of Th1 responses and inc. Th2 responses
21
Q

describe placenta HLA

A
  • placental HLA are almost invariant and very simple
  • identify tissue as human but no other info
  • HLA-G can suppress some leucocytes and down regulate maternal immune responses
22
Q

define conceptus and embryo

A

conceptus: everything resulting from fertilised egg
embryo: baby up to week 8 of development

23
Q

define foetus and infant

A

foetus: baby for rest of pregnancy
infant: after delivery

24
Q

what are the weights of the baby in trimesters?

A

1st: 50g
2nd: 1050g
3rd: 2100g

25
Q

give examples of the chromosomal abnormalities

A
  • too few sex chromosomes = Turners
  • too many sex chromosomes = Klienfelter’s
  • too few autosomes = non-viability
  • too many autosomes = trisomy 21
26
Q

what are the 4 organs that have late development? why?

A
  • lungs
  • digestive system
  • immune system
  • brain
  • have limited use in utero so late development
  • problems developing here become apparent at birth
27
Q

what are the functions of the placenta?

A
  • exchange of nutrients and waste products
  • connection/anchorage
  • separation
  • biosynthesis
  • immunoregulation
28
Q

describe the anatomy of the placenta

A
  • primary subunit = placental villus that has branches
  • provides large SA for exchange b/ maternal and foetal vascular systems
  • veins = oxy blood, arteries = deoxy
  • placenta carries out parallel function to lungs in pregnancy
29
Q

what are cotyledons?

A
  • maternal surface of placenta is sub-divided into cotyledons
  • 30-60/ placenta
  • each contains one or more villi
30
Q

describe the development of the placenta

A
  • approx 9 days post fertilisation, conceptus completely in maternal endometrium
  • placenta originates from cytotrophoblasts layer
  • cytotrophoblasts proliferate into syncytium to form columnar structure
  • this becomes villous structure
  • overall structure then doesn’t change but is modified
31
Q

what are the levels of cytotrophoblasts at term?

A

fewer

so there can be a closer apposition b/ syncytium and placental capillaries

32
Q

describe the contact of the conceptus with endometrial cells

A
  • Early: conceptus contact with endometrial cells
  • as it grows, conceptus makes transient contact w/ maternal capillaries
  • rapidly cytotrophoblasts cells form capsule around conceptus
  • this isolates it arounf 4 weeks PF
  • decidual glands hypertrophy during 1st trimester to provide nutrients for placenta and baby
33
Q

how long does the cytotrophoblast shell remain in place for?

A

until 8 weeks PF

blocks spinal artery formation

34
Q

describe the blood supply formation

A
  • 10-12 weeks GA, cytotrophoblast plugs break down and spiral arteries form to supply foetus w/ blood normally
35
Q

what is the main risk time during pregnancy?

A

if placenta is not anchored properly, there is inc. pressure as it is exposed to maternal blood supply
can lead to detachment and a miscarriage

36
Q

describe the spiral artery remodelling

A
  • cytotrophoblast (ctb) cells remodel sprial arteries during 1st trimester until 16/18 weeks GA
  • remodelling converts narrow bore spiral vessels into wide-bore vessels to transport more volumes of blood
  • ctb cells replace vascular endothelium and VSMCs
  • vessels here cannot respond to vasoconstrictors
37
Q

what are the maternal risks of pregnancy?

A
  • lie in labour and delivery
  • remodelling of spiral artiers (vessels can lose a lot of blood after delivery)
  • placenta checked to see if all been delivered, quite inflexible, any left in uterus may lead to ineffective uterine contractions
38
Q

how is the loss of blood in labour reduced?

A

contractions of uterus after placenta delivery

39
Q

what are the risks to the infant?

A
  • defects to gametes
  • loss of any autosome not compatible with life (miscarriage)
  • changes in sex chromosomes is less severe
40
Q

what are the risks to the placenta?

A
  • incomplete anchorage in 1st trimester
  • once pregnancy passes viability, early delivery problem
  • infants born before 32w GA are greatest risk due to incomplete development of 4 organs
41
Q

what is stillbirth?

A

death of infant within uterus, delivered without signs of life

42
Q

how do you detect stillbirth?

A
  • via monitoring of foetal well being
  • US: monitor foetal movements
  • foetal blood flow assessment: doppler US