Physiology of pregnancy Flashcards
When can bhCG be detected on urine dip to dx pregnancy?
2-3wks
How many weeks does it take to be able to identify intrauterine gestational sac on TVUS?
~5weeks
@5.5 weeks in TVUS you can see the yolk sac within & embryonic foetus identified
When can you detect foetal heartbeat on TVUS?
~ 6 weeks
Pregnancy causes major changes in every bodily system although it is a normal physiological event & everything usually returns to normal after delivery
BUT pregnancy can exacerbate pre-existing conditions & uncover “hidden” or mild conditions such as..?
- hypertension,
- diabetes (prediabetes → gestational diabetes)
Where are the initial pregnancy steroids from?
the maternal ovarian (CL) steroids: initial
From week 7 there are placental peptides. What are these?
hCG (like LH)
hPL (like GH)
GH
What are the placental and foetal steroids?
progesterone
oestradiol
oestriol
What are the maternal and foetal pituitary hormones?
GH,
T3,
prolactin (prepare breasts)
Corticotrophin releasing factor (CRF)
What date is term for a baby?
37 weeks (although you expect ~40)
e.g. preterm is BEFORE 37 wks!
When does progesterone stop being produced by the corpus luteum?
becomes placental from 6-9wks onwards
What does progesterone do in pregnancy?
- causes SMC relaxation “uterine quiescence”
- mineralocorticoid (Na resorption and K and H exretion) effect and CVS changes
- breast development
What does oestrogen in pregnancy cause?
- Feto-placental unit
- [e.g. foetus contributes precursors to some hormones and the placenta finished the hormone development]
- Development of uterine hypertrophy
- Metabolic changes (insulin resistance)
- [for structural and metabolic requirements of foetus and removal of waste productions]
- CVS changes (fluid gain)
- [?for provision of amniotic fluid]
- Breast development
What hormone causes this change in pregnancy?
- increases from T2 e.g. 13-28 wks
- insulin resistance
- & foetal lung maturity
cortisol!
What hormone causes these changes in pregnancy?
- increased from T2 e.g. 13-28 weeks
- possibly involved in initiation of labour
CRH
Corticotrophin releasing hormone
What hormone causes the following changes in pregnancy?
- metabolic changes & insulin resistance,
- some role in lactation
HPL - Human placental lactogen
= similar to GH
Where does prolactin come from in pregnancy?
- Predominantly maternal anterior pituitary
- (anterior pituitary = FLAT PeG)
- increases throughout pregnancy
- breast development of lactation
What are the changes happening with T3/T4/ TSH/TBG in pregnancy and why?
- increase in total T3&4,
- but same free T3/4
- most bound due to raised TBG
- –> thyroxine needed for foetus’s neural development
What rough order do the different hormonesa come into effect to affect pregnancy
- Oestrogen
- Progesterone
- HCG
- Human Placental Lactogen (like growth hormone)
- HCG peak till 13 weeks e.g. 1st trimester
- –> PLACENTAL HORMONES:
- progesterone & oestrogen constantly rising thoughout pregnancy but starts off low
- HPL (like GH) starts from ~10wks onwards
Circulating volume during pregnancy increases 40-50% by the end of T1.
How and why?
E2 & P act on RAAS for
Na+ & water retention, increased BV from ~5L -> 8.5!
retained water includes: foetus, placenta, amniotic fluid, plasma volume, mammary glands, uterine muscle (less rigid), & oedema –> lungs, CT, ligaments, ankles
The normal Haematocrit in non-pregnancy is 130 while in pregnancy it drops to 110-115. What process in pregnancy does this refer to and when should this be tested for?
- the Red cell volume increased during pregnancy but not nearly as much as volume increase (inc. 40-50%) = relative physiological dilution (reference rage TF changes)
- Dont worry in pregnancy if>100.
- Check red cell volume at booking e.g. 12 wks - Hb & electrophoresis, 28wks - when dilution is maximal & 36 weeks
- we check because there is a risk of bleeding during labour & if this is on background of anaemia, problems rise quicker.. we want to optimise health before even if this means transfusing
Why do we not worry about the relative physiological dilution of red cell volume in pregnancy?
it normamlly is ~130 and we dont worry about it unless its <100…
fHb has a higher affinity for O2, so receives it from maternal Hb
HOWEVER: smoking & carbon monoxide –> foetal hypoxia
What are the causes of anaemia in pregnancy e.g. <100? (well 110-115 is normal)–> @ MCV
- Low MCV (TAILS) - <80
- Iron deficiency (taking iron gives constipation, unpleasant GI SE’s –> if really cannot tolerate oral, give IV),
- Thalassaemia/sickle cell (find out at booking - inheritance issue if partner also has)
- High MCV - >100
- B12/folate
- Normal MCV - 80-100
- Chronic disease
- Marrow issue?
- Mixed iron/B12/folate deficiency
besides relative phsyiological dilution of red cell volume due to fluid increasing/retaining water > inc. red cell volume
What other blood changes occur in pregnancy?
- ↑WBCs,
- ↑clotting factors making blood hypercoagulable
Why are heart problems (among other pre-existing/hidden/mild conditions) exacerbated in pregnancy?
- Cardiac output increases 40-50% in pregnancy…
- The CO = SV x HR
- in preg SV increases a lot
- may get slight LVH to a degree on ECG
- and HR a bit (only ~9bpm+)
- overt tachycardia in pregnancy is NOT normal
- Some peoples hearts dont cope with the increase in CO…
- those with underlying heart conditions are at risk
- can uncover or exacerbate a pre-existing problem
BP = CO x TPR
the cardiac output increased 40-50% in pregnancy due to ++SV (CO=SV xHR).
therefore, What happens to BP in pregnancy?
TRICK! BP decreases in pregnancy… it normalises towards the end of pregnancy
because BP = CO x TPR and TPR DECREASES
=> progesterone is a smooth muscle relaxant –> vasodilation
increased flow to uterus, placenta, muscle, kidney, skin (neoangiogenisis)
check BP at booking 12wks & always BP and urine dip a pregnant woman!
why must you always BP and urine dip a pregnant woman?
- pregnancy induced hypertension if >20wks
- Pre-eclampsia (PET) if HTN and proteinuria >2O wks
- => tend to have blunted drop in BP to start with then a rapid increase in BP as PET develops.
- Commonly PET arises right at end of pregnancy e.g. 39 wks
A patient is 18 weeks pregnanct and has high BP and protein uria. What does this mean?
HTN & renal disease if <20wks
if >20wks then its pregnancy induced hypertension and PET
NB: BP decreases and then normalises towards the end of the pregnancy
A patient is 22 wks pregnant with high BP and proteinuria, what is the cause?
- if >20wks then its pregnancy induced hypertension and PET
- NB: BP decreases and then normalises towards the end of the pregnancy
- high BP and proteinuria = HTN & renal disease if <20wks
What are the risk factors for PET?
Prevalence of PET is 2-4%;
10% have some hypertensive problem.
- HTN/renal disease/PIH
- Primiparity (1st pregnancy)
- Previous PET (especially early onset or severe)
- Obesity
- Multiple pregnancies
- Afro-Caribbean women
What blood tests should be done for PET?
FBC, U&E, renal, LFT, clotting (reflects end-organs affected)
protein:creatinine (PCR if raised = significant ,in terms of being nephrotic range proteinuria)
What test can expanding uterus change?
ECG changes due to expanding uterus
Metabolic changes occur in pregnancy. What are these?
- Lay down stores (anterior abdominal wall, which is used later in pregnancy & in puerperium)
- make transfer across placenta as efficient as it can be (e.g. increasing gradient)
Metabolic changes occur in pregnancy.
Pregnant women should eat for two. True or False?
False. Do not need to eat for 2.
Basal metabolic rate rises 350kcal/day in mid gestation e.g. >20wks, -> only need the equivalent of an extra mars bar a day
250kcal/day in late gestation –> 75% to foetus & uterus, 25% to respiration
Metabolic changes occur in pregnancy.
When should pregnant women be weighed and what is the weight change expects?
Weight gain of approximately 10-14kg
- Only weigh people at booking (12wks) now
- Total 10-14kg =
- 5kg (foetus & placenta)
- 4.5kg (fat & protein - anterior abdo wall, liver, muscle)
- 1.5kg (body water) +
- 1kg (breasts)
- 0.5kg (uterus)
What does the progressive rise in cortisol, HPL and E2 across pregnancy do for metabolism?
These rise and cause progressive insulin resistance across pregnancy.
BUT the basal insulin level rises in response to keep sugars normal (hyperinsulinaemia) – if their pancreas is good enough to keep up
- the insulin resistance helps to lay down fat stores (water, foetus and placenta, fat on: liver, abdo wall and muscle & breasts and uterus) and create glucose concentration across the placenta
- babys sugars mirror their mums - babys dont need to make insulin
Which trimester of pregnancy does this change occur in?
- hPL causes insulin resistance (not “diabetes”, but pre-diabetics experience gestational diabetes)
- ↑serum glucose, more crosses placenta
The 2nd trimester of pregnancy for foetal reserves (>13wks)
What trimester do these changes occur in?
- ↑insulin from pancreatic β cells
- Anabolism & glucose into tissue stores
- ↓serum glucose
these are building the maternal reserves and this happens in the first trimester of pregnancy
<12wks
Increased oxygen consumption is needed in pregnancy. How is this achieved?
- pregnant women breathe more DEEPLY - their minute volume increases 40% (e.g. increased gas exhaled/inhaled from persons lung in one minute)
- increased resp centre sensitivity to CO2
- increased displacement of ribcage upwards
- (breathing deeper > not noticeably more frequently)
-
increased PO2 and decreased PCO2 facilitates placental gas transfer
*
What happens to a pregnant womans appetite/thirst and gut motility?
in pregnancy there is increased appetitie and thirst
there is decreased gut motility => progesterone relaxes SMC! (along with mineralocorticoid effect and CVS changes & breast development)
- –> constipation,
- –> LOS relaxation and acid reflux (also from up-pressure from uterus)
(oestrogen develops breast and cvs changes too but also uterine hypertrophy and metabolic changes e.g. insuling resistance)
Why are pregnant women more prone to increased UTIs?
SMC relaxation of urinary tract
- progesterone relaxes SMC
Why do pregnant women pee more?
- ↑urination (& clearance of creatinine, urea, ureic acid) due to
- ↑blood flow (vasodilation) to kidney & filtration
- ↑fluid in body (foetus, placenta, amniotic fluid, plasma volume, mammary glands, uterine muscle, oedema)
- Expanding uterus presses on bladder
What are the different parts of the uterus?
- fundus -
- uppermost thicker muscle –> push out
- corpus -
- lined by decudia, vascular –> survival of baby + helps push out
- Isthmus (lower segment) -
- full formed at 36 wks, circular and longitudinal smooth muscles.
- Muscle tone & sotened pelvic floor muscles allows presenting part to move to lower segment @36weeks –> path out uterus
- Cervix = effaced and dilated during labout, mucous plugs stops ascending infection (+acidity of vagina)
What are the uterine changes?
- ↑muscle mass & blood flow (oestrogen effect) – top e.g. as fundus needs to push out
- Thin funnel & passage out for foetus – lower uterine segment (cut here in caesarean sections!)
- muscle tone & softened pelvic floor muscles allows presenting part to move to lower segment at 36weeks –> path out uterus
What is the function of the cervix?
How do changes help this?
function of cervix is to retain pregnancy
- ↑vascularity
- Prepares for expansion:
- tissue softens,
- CT breakdown
- Proliferation of glands & mucus: anti-infective (stops ascending infection; along with acidity of vagina)
How does the body start to return to normal after pregnancy?
rapid fall in steroids on delivery
(e.g. as progesterone, oest and oestrdiol etc become placental from 9w onwards)
- –> Endocrine-driven changes return to normal rapidly
- Uterine muscle rapidly loses oedema but never returns to pre-pregnancy size
- Prolactin action on breast INCREASES!
