pregnancy Flashcards

1
Q

what are the weeks for the trimesters of pregnancy and what are the changes through these *

A

term 1 - 0-13wks

13-26wks

26-39wks

maternal changes occur throughout

baby is embryo at start, by end of 1st trimester is fetus and viable by 26wks w/o intensive care unit, at term at 39wks

placenta changes are complex and mainly occur in 1st half

the trimesters are made by experience not science - if get past 1st trimester it is likely that the pregnancy will continue

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2
Q

what are the maternal physical and anatomical changes in pregnancy *

A

at end of trimester 1 - cant necessarily tell from appearance that pregnant

in 2nd and 3rd trimester the baby grows fast

angle of back changes = ache and pain

Increased weight [3rd]

Increased blood volume [2nd & later] - more material is needing to be fed from maternal blood

Increased blood clotting tendency [2nd & later]

Decreased blood pressure [2nd]

Altered brain function [1st & later] - because exposed to high levels of steroids, varies between people

Altered hormones [1st & later]

Altered appetite (quantity and quality) [1st & later] – GI imbalance - bump so less space for stomach so smaller meals and eat more often

Altered fluid balance [2nd & later] - kidney goes into overdrive, drink more - linked to the increased blood vol

Altered emotional state [1st & later] - can be elated or depressed

Altered joints [3rd] - more flexible (eg pelvis has to chamnge shape to let the fetus out)

Altered immune system [1st & later] - change to allow pregnancy to continue and remain resistant to disease

morning sickness - doesnt just occur in the morning

the extent of the changes occur at differnt times in the 9months - so need to knwo the way that timings in pregnancy are organised

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3
Q

describe the maternal hormonal changes in pregnancy *

A

much higher hormone levels than experienced in menstruation

HCG is released from placenta - peak in trimester 1 (starts to rise before the end of the menstrual cycle, a week after implantation) stops bleeding and acts on the corpus luteum to keep progesterone and oestrogen production

HCG falls after first trimester but is still present

maybe HCG is related to morning sickness because that is also mainly in 1st trimester - maybe wome affected have a higher sensitivity to HCG

oestrogen, progesterone and placental lactogen increase towards the end of pregnancy - they mirror the increased size of the placenta

low progesterone levels = loss of fetus at any stage in pregnancy

the high levels of steroids suppress the HPG = low LH and FSH = no cyclic uterine/ovarian functions

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4
Q

when is the main risk to the mother’s health *

A

delivery - remodelling of teh spiral arteries mean the vessels can lose large volumes of blood in birth - limited by contraction of the uterus after placenta has been delivered

must check no placenta missing - inflexible so any left in uterus will prevent contraction = blood flow into uterine lumen

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5
Q

define conceptus *

A

everything resulting from the fertilised egg - baby, placenta, fetal membranes, umbilical cord, amniotic fluid and chorion

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6
Q

define embryo *

A

the baby before it is clearly human

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7
Q

define fetus *

A

the baby for the rest of pregnancy - when it is clearly human and still in uterus

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8
Q

define infant *

A

less precise - normally applied after delivery

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9
Q

describe a blastocyst *

A

at 9days

contains a disk in the middle

developed from the egg

has 2 layers of cells in it

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10
Q

where does embryo and fetus make RBC

A

liver - no limbs with bones

(fetus will have limbs and embryo might have buds but cant make RBC)

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11
Q

what is the difference in time frame of pregnancy and embryology *

A

pregnancy is the 1st day of last period - done because the mother can identify this easily

embryology times are from time of fertilisation

implication is that when premature babies are delivered 2wks makes a difference to their chance of survival - if very young resus is not done because it would give them a severe handicap/they wouldnt live

at term the 2 weeks doest make much difference because term is 37-41 wks

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12
Q

how can we look at pregnancy *

A

observe it with MRI or US

measurements can be made of circulating factors in the mother’s blood, or dimensions

ethics of research into this makes it difficult to know how the measurements fit into development of the baby

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13
Q

what is the benefit of embryos from different species looking similar

A

can look at what is likely to be happening in humans

eg eye development in fish - expect genes of same family to be present in humans

therefore some careful conclusions can be drawn - cant overestimate

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14
Q

how does gestation time vary between species

A

usually smaller animals = smaller gestation time

not always the case

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15
Q

describe how teratogens interfere with development *

A

the more rapidly developing tissue is more suseptible to damage

teratogen = any factor that damages development

CNS is vulnerable throughout pregnancy

heart, limbs, palate and ear are more suseptible in trimester 1

external genitalia are vulnerable from late 1st throughout

most of the major congenital abnormalities happen in 1st trimester, with functional abnormalities and minor congenital anomolies happening later

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16
Q

how does maldevelopment help our understanding

A

helps us identify when things are most vulnerable and which bits are

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17
Q

describe the placenta *

A

it is a disk 20cm across

the foetal membrane is the thin tissue around the outside, it encloses the amniotic fluid which surrounds the baby and keeps the baby safe

umbilical cord carries waste from the baby to the mother’s circulation and nutrients to the baby

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18
Q

describe the maternal side of the placenta *

A

contact point between fetus and mother - in direct contact with the maternal blood

subdivided into 30-60 cotyledons - they vary in size and are a subdivision of the placenta - the gaps between them are made by the maternal tissue behind the uterus

each cotyledon contains at least 1 villus

the cotyledons are bigger in the middle and smaller at the edge

the size and number doesnt affect how well the placenta does

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19
Q

describe the basic placental structure *

A

maternal arterioles contain oxygenated blood - supply blood to the foetus

maternal blood leaves through the venule

the maternal and fetal blood dont come in contact

the deoxygenated fetal blood comes from the umbilical artery (comes from heart) and enters a villus - a highly branched structure to increase the SA (11m sq)

arterial and venous vessels are connected to smaller capillaries ion the terminal parts of the villus

nutrients and oxygen are exchanged with the mother’s blood and the oxygenated fetal blood leaves through the umbilical vein

the highly branched villus tree also anchors the placenta securely for the pregnancy

there is intimate contact between fetal and maternal tissues - making interesting immunology

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20
Q

what are the functions of the villus/placenta *

A

separation of maternal and fetal blood

exchange between the vascula systems

biosynthesis - makes HCG, oestrogen, progesterone and placental lactogen

immunoregulation - contain Ag on surface that indicate that the tissue is human but not which human - hardlyany HLA variation on the placenta. Know that placenta is important for immune reg because in ectopic pregnancy with placenta, baby is still protected from mother’s immune system

connection - placenta connected to maternal decidua otherwise fetus is lost

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21
Q

describe placental development *

A

at day 9 PF teh coinceptus is implanted into the maternal decidualising endometrium

the outer layer of conceptus are multinucleated syncytiotrophoblast whcih contains fluid called lacunae

the underlying layer of cytotrophoblast is proliferating next to embryo - this is where the placenta develops

following implantation the cytotrophoblast proliferates into the syncytium - 1st a columnar structure is formed (cytotrophoblast column) whihc then undergoes branching (villus sprouts)

at centre of each villus are mesenchymal (extra-embryonic mesoderm) cells from which the villus vascular system develops

inbetween the villus stems are the intervillus spaces that develop from the syncytial lacuna

branching continues

at term there are fewer cytotrophoblast so there can be closser connection between the syncitium and capillaries - maximise nutrient transfer and enhance fetal growth in later pregnancy

placenta is 5cm across at this stage - in 2nd and 3rd trimester grows to 20cm - because of increased branching

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22
Q

describe how the contact of the placenta changes during pregnancy *

A

at earliest stages of pregnancy conceptus is in contact with endometrium

in early embryo development, the cytotrophoblast shell limits the blood and oxygen going to the embryo by 4wks - so that there isnt a high level of flow - this is because the rapidly dividing cells in trimester 1 are especially suseptible to oxygen free radicals - so less oxygen at this stage is safer

teh decidual glands hypertrophy during 1st trimester - provide nutrients for the placenta and devloping baby - placenta is the soutrce of the nutrients (histotrophic nutrition) rather than maternal blood

the cytotrhopblast shell remains in place until about 8weeks post fertilisation - spiral arteries are blocked

the maternal blood is supplied to the placenta through the spiral arteries - at 8wks they are remodelled by cytotrophoblasts that infiltrate them and remove their sm and underlying epithelium from periphery 1st then centre (cyrotrophblasts replace the epi and sm) - begins during 1st trimester and continues to 16-18wk

now maternal blood supplies nutrients (haemotrophic nutrition)

baby grows dramatically in the second and third trimester - a lot of blood is needed from the mother

the remodelling of the spiral arteries widens the blood vessels (because they cant contract becausse the sm has gone) so large volumes of blood and nutrients can go to the fetus = increase in rate of growth

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23
Q

what are the effects of placental maldevelopment *

A

miscarriage in early/late 1st trimester if the baby is not anchored correctly

miscarriage in 2nd trimester - rare

pre-eclampsia - early delivery - when placenta doesnt work properly

fetal growth restriction - small infant

24
Q

when are fetuses viable *

A

26-27 weeks (end of 2nd trimester) w/o ICU

22 weeks absolute limit

25weeks 50% survival

25
Q

define ‘term’ *

A

the expected timing of delivery

normally 40 wks ie 280 days from 1st day of last menstrual period

but coplvers 37-41 weeks

26
Q

define preterm *

A

delivery <37wks

27
Q

define post term *

A

delivery >41 weeks

28
Q

describe the weight gain in pregnancy *

A

variable

10-15Kg - include the weight of the fetus, amniotic fluid and placenta, increased fluid retention, increased nutritional stores

they occur in second, and mainly 3rd trimester

29
Q

descrieb the source of progesterone through pregnancy *

A

from fertilisation to 8weeks - corpus luteum - this si sustained by hCG - by 6wks it produces less and by 9 it stops completely making any steroidds

placenta also makes progesterone - in early weeks small so contribution is limited

by 10 wks placenta only source - produces increasing levels for the rest of pregnancy

this is the luteo-placental shift

30
Q

source of oestrogens during pregnancy *

A

in early wks corpus luteum also produces oestrogens - 17B-ostradiol

by the luteo-placental shift the oestrogens are produced by the fetal adrenal glands and the placenta

placenta doesnt express the enzyme that converts pregnenolone to androgens so this occurs in adrenal glands (developed in 1st trimester)

the weak androgen produced (dehydroepiandrosterone, DHEA) is sulpfated = DHEA-S this is inactive - female fetus is not exposed to androgen in development

DHEA-S circulates the placenta - converted to 17b-oestradiol

there are also high levels of oestriol produced by hydroxylation of DHEA-S in fetal liver to make the precurser 16OH-DHEA-S

31
Q

describe the increased blood clotting tendancy of mother 8

A

starts early

greatest at term - protective

also may be important in the interactions between the placenta and maternal blood throigh pregnancy

32
Q

describe the decreased BP *

A

lowest in 2nd trimester

increases fainting risk

rises in 3rd - but still lower than hypertension - 120/70 normal

33
Q

describe the increase in basal temp *

A

by 0.5degrees after ovulation, this reverses during menstruation and into 1st trimester - probably because of progesterone

as fetus increases in size - contributes to maternal temp - may exceed 30degrees

34
Q

describe the increased breast size *

A

human placental lactogen, prolactin, oestrogens involved

changes start in 1st trimester and continue - greatest at end

35
Q

describe changes in vaginal mucus secretion *

A

increased

clear

if bloodstained, coloured, or has offensive odour - medical advice should be sought

36
Q

describe morning sickness *

A

nausea and vomiting can happen at any time in day

can be severe = weight loss

severe form is hyperemesis gravidarium

highest incidence in 1st trimester

37
Q

decribe altered brain function *

A

high levels of steroids alter brain func - esp prog

size decreases slightly - might be insignificant

38
Q

describe the altered fluid balance and urination freq in pregnancy *

A

increased fluid retention and higher plasma vol - 50% higher by end

urinary freq increases in 1st, normal in 2nd, increases in 3rd trimester

chnages in 1st due to changes in hormones regulating altered kidney func

by 3rd - the uterus is exerting pressure on the bladder

39
Q

describe the altered emotional state *

A

change in hormones

variable

glow/emotional/depressed leading to post-natal depression

or pregnancy positive experience but afterwards get post-natal depression

40
Q

describe the changes in the joints *

A

more flexible - continues after pregnancy

41
Q

describe the altered immune system *

A

factors that suppress the immune system are made at utero-placental interface - decrease the Th1 and increase Th2 system - changes are subtle but co-operate to have effect

express HLA-G only has 5 variants and is a simplistic structure - human marker but not which human. HLA-G can suppress activity of leukocytes and down-regulate the maternal immune system in the uterus

42
Q

what can effect the early satges of development *

A

teratogens - structures will be there but details effected

spina bifida nad cleft palate occur at early stage

43
Q

risks in the 2nd trimester *

A

few

44
Q

risks in the 3rd trimester *

A

associated with birth

lungs, digestive system, immune system and brain develop late - in preterm infant might not hve developed properly = death/illness

45
Q

what are the 2 different meanings of embryo *

A

during week 1 PF - means all cells

after this means inner cells of the blastocyst

46
Q

function of each trimester *

A

1 - development

2 and 3 - growth

47
Q

features of first trimester *

A

wk2 - development of bilaminar disk

3- formation of trilaminar disk (mesoderm), CNS and somites, bv infiltration , formation of placental villi (3mm)

4 - closure of neural tube, heart, face and arm initiated, umbilical cord, elongation of placental villi 4mm

5 - face and limbs continue, villi 5-8mm

6 - face,e ars, hands, feet, liver, bladder, gut, pancreas 10-14mm

7 - face, ears, fingers, toes 17-22mm

8wk - lungs, liver, kidneys 28-30wks

all in low o2 env

48
Q
A
49
Q

why is the cyrotrophoblast plug breaking down risky *

A

if placenta not anchored properly it will be lost by the increased pressure

this is late 1st trimester

50
Q

nervous system of the placenta *

A

there is no nervous system - so not regulated by constrictors

feels no pain during delivery

umbilical cord can be cut with no harm to the fetus

51
Q

regulation of placental growth *

A

regulates own growth and development through autocrine mechanisms

maternal decidua modulates placental growth so it is optimal for the mother and fetus

52
Q

risks to the infant *

A

defects in gametes (chromosomes

53
Q

risks with/because of the placenta *

A

if not anchored properly = loss (miscarriage if non-viable, or early delivery) - most common in 1st trimester

some will be due to development problems, others will be due to detachment in late 1st trimester

FGU and PET mean babies are delivered early

infants born <32wks risk because surfactant, digestive system, brain and immune system hasnt developed properly

54
Q

differentiate very preterm from preterm *

A

very is <32wks

preterm is 32-37

55
Q

define stillbirth *

A

teh death of an infant in the uterus, so that it is delivered without any signs of life

definitions vary

one is that if non-viable = miscarriage (<23wks), viable = stillborn

been linked to labour but many cases occur before delivery

can occur at any time - including temr

56
Q

how can you detect still birth *

A

depends on monitoring fetal well being

a decrease/lcak of fetal movements = increased risk

US and fetal doppler is used

if fetal comprimise is detected - need C section asap

57
Q

causes of stillbirth *

A

50% in labour - need to monitor pregnancy because

some studies say risk is higher in subsequent pregnancy