Pregnancy Flashcards
1
Q
What are the terms used to describe the timing of pregnancy?
A
Last menstrual period
- convention
- counted from the first day of the last mentrual period
Gestational age
- LMP + 2 weeks
- start from the point of fertilisation - right after ovulation
Accurate dating → importance in preterm babies
- in UK a baby with GA > 24 weeks would always be revived and treated a very positively
- whereas a baby of lower gestation (eg 22 weeks) would be considered borderline for survival, and a clinical decision whether to treat or not would be taken.
2
Q
What is the 1st trimester?
A
Weeks 0-13
3
Q
Define the features and risks of the first trimester.
A
- Maternal changes
- N+V “morning sickness”
- Hard to tell someone is pregnant
- Increased urinary frequnecy due to hormonal changes
- Most embryological development takes place in this period - focus on structural development not growth
- Risks - Most dangerous time for the foetus, due to:-
- Most susceptible to insult/ teratogens - congenital abnormalities
- e.g. Spina bifida, Cleft palate
NOTE: main development of lungs, the digestive system, the immune system and the brain happens late in pregnancy (they do start developing in early stages though)
- Chromosomal abnormalities - miscarriage
- e.g. Turner’s (XO), YO inviable, Kelinfelter’s XYY, Down’s trisomy 23
- Placental problems - miscarriage
- e.g. weeks 10-12 when placenta becomes less anchored as cytotrophoblast plug breaks down
- Miscarriage risk highest - 1/3 of all conceptions do not complete the first trimester
4
Q
What is the 2nd trimester?
A
Weeks 14-26
5
Q
Define the features and risks of the second trimester.
A
- The foetus becomes viable (foetus can survuve if born) in this trimester
- 24 weeks = Viability limit
- 25 weeks = 50% survival
- 26-27 weeks (end of trimester) = without intensive care
- However, survivial of preterm birth is often associated with morbidity in premature infants
- Foetal changes
* Focuses on foetal growth (though less than 3) - clear cut increase in foetal weight from 1 → 2 - Maternal changes
- Urinary frequency normalises from first trimester
- Mother starts to feel baby moving
- Risks
- Stillbirth
- Increase in maternal blood clotting tendency
- Maternal blood pressure is lowest during the second trimester, and increases the risk of maternal fainting – so pregnant women should not stand for prolonged periods of time
6
Q
What is the 3rd trimester?
A
Weeks 27-39
7
Q
Define the features and risks of the third trimesters.
A
- CONCENTRATED foetal growth (~2kg)
- Maturation of brain, immune system, lungs and digestive tract (BILD)
- Maternal changes
- Increased urinary frequency as uterus pushes on bladder
- Increases in weight (concentrated particularly in the third trimester - to feed the baby after delivery)
- Risks
- Highest risk to mother at this time
- Gestational diabetes
- Preeclampsia - less blood to foetus - less growth
- Foetal
- Preterm labour
- Preterm premature rupture of membranes
- Placental previa + placental abruption
- Intrauterine growth restriction
8
Q
Define term in pregnancy.
A
- Term (39-40 weeks) is the expected timing of delivery.
- Covers gestational ages from 37 – 41 weeks of gestation, with deliveries either side of these limits being ‘preterm’ or ‘post-term’ respectively
9
Q
Define the following terms:-
- Conceptus
- Embryo
- Fetus
- Infant
A
- Conceptus – everything resulting from the fertilised egg (baby, placenta, fetal membranes, umbilical cord)
- Embryo – the baby before it is clearly human
- Fetus – the baby for the rest of pregnancy
- Infant – less precise, normally applied after delivery
10
Q
What are the main risk in pre-term infants and why?
A
- In a preterm infant, the 4 main organs or systems (lungs, the digestive system, the immune system and the brain) may not function correctly, and thereby cause illness or death to the infant
- This is because the fetus has limited need of them in utero - so they develop relatively late in pregnancy, during the last few weeks
11
Q
What are the maternal anatomical and physiological changes associated with pregnancy?
A
KNOW CHANGES EXPLANATION FOR UNDERSTANDING
First Trimester
- Altered emotional state - changes in hormone levels within the maternal system
- Altered endocrine system
- Altered brain function - high levels of progesterone (well established that many steroids affect brain function in humans generally)
- Altered Immune system - need to accomodate non-self entity
- factors produced at the utero-placental interface to suppress the maternal immune system
- placenta expresses invariant (unlike the others which are highly polymorpic),and structurally simplistic HLA-G:-
- immunological signal that shows that the tissue is human – but little or no information on which human it is from (not as being ‘non-self’) in addition
- suppress the activity of some leukocytes and can down-regulate the maternal immune system within the uterus.
- Altered appetite
- increase size of uterus imposes increasing pressures on GI - decrease the distensibility of the stomach
- N and V
- co-incides with the highest levels of hCG in the maternal circulation
- decline in hCG during second trimester improves symptoms
- Increased Breast size
- increased hormone levels in the maternal circulation (human placental lactogen, prolactin, and ostrogens are all involved)
- start in the first trimester and continues through
- Fluid balance + urination frequency
- enlarged uterus will be exerting pressure on the bladder, decreasing the maximum size and volume of urine
- Increased basal body temp
Second Trimester
- Decreased Blood pressure - increases the risk of maternal fainting
- Increased blood clotting tendency
- starts early in pregnancy, and is greatest at term
- protective against losing too much blood at delivery
- also due to interactions between the placenta and maternal blood throughout pregnancy
Third Trimester
- Increased Weight
- weight of the fetus, amniotic fluid and placenta, increased fluid retention, increased nutritional stores
- Joints
- maternal pelvis changes to make the connections between the bones more flexible and permit the delivery
- same permanent modification in other maternal joints (persist after pregnancy)
12
Q
Draw a graph showing the hormonal changes in pregnancy.
A
DIAGRAM (past question)
Human Chorionic Gonadotrophin (hCG)
- shows peak levels in maternal plasma in the first trimester, and declines thereafter
- produced by placenta
- rescues the corpus luteum
- acts at the LH receptor to produce oestrogen and progesterone
Steady Increase
Human placental lactogen
- parallel the increased size of the placenta
Progesterone
- very high levels → of particular importance in allowing the pregnancy to continue.
- low progesterone levels, or administration of a progesterone antagonist, will lead to loss of the pregnancy at all gestational ages.
Porgesterone + Oestrogen
- high levels suppress HPG
- very low levels of LH and FSH throughout pregnancy
- no cyclic ovarian or uterine functions
13
Q
How is steroidogenesis an example of the three-way interaction in pregnancy?
A
NOTE: this answer also covers what the sources of progesterone and oestrogens are during pregnancy
- First 9 weeks*
- HcG produced by the placenta rescues the corpus luteum and acts on the LH receptors to produce oestrogen and progesterone
Luteal-placental shift (week 6-9)
After 9 weeks
- Placenta produces an excess of progesterone
Oestrogen formation required all 3 components - (1) maternal adrenal glands (pregnenolone), (2) foetal adrenal glands and/or liver, (3) maternal placenta
- Placenta lacks CYP17 (17αhydroxylase) for conversion of pregnenolone to androgens
- The pregnenolone passes into the foetus - its adrenal gland has CYP17, which converts pregnenolone → dehydroepiandrosterone (DHEA) —sulphation→ DHEAS
- DHEAS can be either:-
- (1) deconjugated in the placenta and form oestradiol and oestrone or
- (2) hydroxylated in the foetal liver to form 16α-hydroxy DHEAS → converted into oestriol in the placenta
14
Q
Describe the main structural features of the human placenta.
A
- 30-60 cotylendons on the maternal side of the placenta
- Each cotyledon contains one or more villi, with larger cotyledons containing more villi.
- The variability in the shape and size of cotyledons does not affect placenta function.
- Placental villous tree - complex branched structure
- provides large SA for exchange between the maternal and fetal vascular systems
- provides anchorage to the maternal decidualised endometrium
- Complex blood supply within each villus - countercurrent flow
- spiral arteries → blood supply
- umbilical arteries (de-oxygenated blood); umbilical veins (oxygenated)
- these larger vessels are connected to smaller capillaries in the terminal portions of each villus
- Despite being in close proximity, maternal and fetal blood supplies are separated from each other
15
Q
What are the functions of the placenta?
A
-
Separation
- prevents mixing of maternal and foetal blood despite the close contact between the tissues
- Exchange of nutrients (maternal to fetal) and waste products (fetal to maternal)
-
Biosynthesis
- Hormones and Growth factors are actively produced
- Functions as a “transient hypothalamo-pituitary-gonadal axis
-
Immunoregulation
- ensures that there is no rejection of the conceptus
- placenta (rather than the uterus) is the key tissue → occasional survival of ectopic pregnancy until delivery shows that the uterine lining is not completely essential for pregnancy
-
Connection (or anchorage)
- placenta makes strong connections with the underlying maternal decidua to last for the 9 months of pregnancy.
- anchorage is essential as the placenta is in contact with maternal arterial blood
16
Q
Summarise the development of the human embryo.
A
I.e. 1st TRIMESTER
1st week after fertilisation
- mitotic (cleavage) division deriving their nutrients from the secretions of the Fallopian tube (by day 6)
2nd week
- Implantation of conceptus (by day 10)
3rd week
- “Development of villi and anchoring”
- Contact with maternal tissues
- Hypertrophy of decidual glands
- histotrophic nutrition (before haemotrophic when cyctotrophic plug break down during late 1st trimester)
6th week
- Start of spiral artery remodelling (1st wave > last up to 2nd wave during late 1st trimester > end with invasion up to decidua)
Start = 12-14 week (2nd wave of spiral artery remodelling), End within 4 weeks
- Invasion up to the myometrium
- Break down of cytotroblast plugs and haemotrophic nutrition
17
Q
Detail the development of the placenta.
A
- Implantation of conceptus
- trophoblast → placenta
- cytotrophoblast is surrounded by syncitioblast
- trophoblast → placenta
- Development of villi and anchoring - CONCEPTUS INVASION
- primary villi = cytotrophoblast invades into synctioblasts
- secondary villi = extra-embryonic mesoderm (NOT OF FOETUS!!!) invades into cytotrophoblast layer
- tertiary villi = branches of the umbilical artery and umbilical vein grow into the mesoderm → vascularization
- Endometrium undergoes decidualisation
- Hypertrophy of decidual glands
- histotrophic nutrition = nutrition form the maternal decidual gland until end of 1st trimester as conceptus is not in contatc with maternal aterial blood
- Spiral arteries
- Spiral arteries open to form funnel shaped openings to allow trophoblast entry
- Decidualised endometrium also mediates the invasiveness of trophoblast cells and triggers remodelling of spiral arteries
- Cytotrophoblasts
- invade spiral arteries (same molecular mechanisms as tumors, but are highly regulated and controlled)
- remodel:
- destroy the smooth muscle and elastic layers and replace them with fibrinoid material → no longer vasoconstricts → narrow vessels widen to carry more blood to placenta
- line vessels with trophoblast
- Contact with maternal tissues
- endometrial contact
- brieft contact with maternal capillaries and then cut off by cytotrohphoblastic shell
- Cytotrophoblast plug gradually breaks down to expose placenta to maternal blood → haemotrophic nutrition (end of 1st trimester)
18
Q
Describe a pathology regarding spiral artery remodelling and its consequences.
A
- Spiral arteries do not open properly
- Invasion depth up to decidua
- 30–50% of the spiral arteries of the placental X undergo remodeling
- Poor placental perfusion
- Clotting in the uterine arteries
- Vessel contraction
- Causing →
- maternal : hypertension (BP > 140/90, 300mg protein/ day measured in 2 occasion); eclampsia (>1 convulsions from high blood pressure, often followed by coma)
- foetal : IUGR, HELLP syndrome, preterm birth
