pregnancy physiology Flashcards
mechanical adaptations to pregnancy
centre of gravity is no longer over feet
pregnant person needs to lean backwards and the curves of the spine change along the whole length
consequences of shift in centre of gravity for pregnanc women
more prone to back pain during and after pregnancy
what is relaxin
hormone produced during pregnancy
effects of relaxin, increased levels of oestrogen and progesterone
increased pliability and extensibility of connective tissue
ligamentous joints become less stable
symphysis pubis and sacroiliac joints are particularly affected
how much does the pubic symphyseal gap increase by
normally 4-5mm
increases on avg 3mm
what is symphysis pubis dysfunction
group of symptoms that cause discomfort in the pelvic region
usually occurs during pregnancy, when your pelvic joints become stiff or move unevenly.
when does joint loosening occur during pregnancy
as early as 10wks
when does joint loosening return to normal
4-12wks post partum
how much does the load on the hips increase during pregnancy
at term there is an increased load on the hip joints 2.8x the normal value when standing
how does the basal metabolic rate change during pregnancy
increases
why is metabolism altered during pregnancy
to ensure adequate nutrition for foetal growth
insulin and pregnancy
relative insulin insensitivity
human placental lactogen (from placenta) acts against maternal insulin
storage of lipids in pregnancy
increased storage of lipids in maternal tissues
FAs are vital for development of foetal organs
normal weight gain during pregnancy
10-14kg gain throughout pregnancy
what is gestational diabetes
high blood sugar (glucose) that develops during pregnancy and usually disappears after giving birth
fatigue during pregnancy
can be overwhelming during the 1st trimester
tends to get better in the 2nd trimester
often returns towards the end of the pregnancy - increased work load, discomfort and difficulty sleeping
why does fatigue occur during pregnancy
hormonal changes
why does heartburn and reflex occur during pregnancy
food moves more slowly into the stomach
delayed gastric emptying
relaxation of lower oesophageal sphincter
mechanical pressure from enlarged uterus
why is GA risk higher during pregancy
increased risk of gastric reflux
higher risk of aspiration and increases with advancing pregnancy
what % of pregnant people develop oedema
80% develop some oedema
particularly towards term
why does oedema develop during pregnancy
physiological sodium and water retention
decreased ability to excrete a sodium and water load
increased blood vol and decreased venous returin (IVC compression)
what can oedema be a sign of
pre-eclampsia
what is pre-eclampsia
a condition in pregnancy characterised by high BP sometimes with fluid retention and proteinuria
breast changes in pregnancy
increase in size and vascularity become warm, tense and tender increased pigmentation of areola and nipple 2y areola appears montgomery tubules appear on the areola
when can colostrum like fluid be expressed
from the end of the 3rd month
changes in thryoid hormone levels during pregnancy
liver produces more thyroid binding globulin
total level of T4 and T3 also increase so free T3 and T4 stay the same
iodine and pregnancy
pregnancy is associated with a relative iodine deficiency
maternal iodine requirements increase
why are maternal iodine requirements increased
iodine is actively transported to the fetoplacental unit and urinary iodine excretion is doubled because of an increased glomerular filtration rate and decreased renal tubular reabsorption
why might the thyroid gland hypertrophy during pregnancy
gland works harder to increase its’s iodine uptake
may hypertrophy to ensure adequate levels of iodine are trapped
why is hyperemesis gravidarum associated with biochemical hyperthyroidism
the beta sub unit of BHCG is very structurally similar to TSH
betablockers can be used to control tachycardia caused by high T4 levels
biochemical hyperthyroidism will resolve with hyperemesis
how common is thyrotoxicosis in pregnancy
1/500 pregnancies
most often due to Graves (AI)
TSH receptor antibodies can cross the placenta and cause foetal +/or neonatal hyperthyroidism
how common is hypothyroidism in pregnancy
1%
why is good thyroid replacement important in pregnancy for hypothyroidism
foetus is dependent on maternal thyroid function until foetal thyroid function begins ~12wks gestation
immunosuppression in pregnancy
general state of immunosuppression to allow for foetal tolerance
this increases maternal susceptibility to infection
explains why some AI conditions can improve during pregnancy
why does the maternal heart have to work harder during pregnancy
growing fetus
weight gain associated with pregnancy
increased oxygen requirements of uterus and breasts
also has to pump blood through the utero placental circulation
why is cardiac disease important to consider during pregnancy
people with cardiac disease can suffer significant complications during pregnancy
can result in maternal and fetal death
previously undiagnosed cardiac disease may come to light
by how much does the circulating blood volume increase during pregnancy
by 50-70% of the non-pregnant
what causes the physiological anaemia during pregnancy
RBC mass increases but only by ~40%
causes a relative haemodilution
why is EDV increased during pregnancy
increase in circulating blood vol
increased L ventricular and EDV
can be seen as early as 10wks on ECHO
why can increased circulating blood vol be a problem during pregnancy
can cause issues for those w/ dilated cardiomyopathy or other lesions (e.g. mitral stenosis, pulmonary HT)
resistance of the the peripheral vasculature during pregancy
falls
at its lowest between 20-32wks
equation for systemic vascular resistance
SVR = (MAP-MVP)/CO
changes to SV during pregnancy
drops
due to increased circulating vasodilators and diversion of blood into the low pressure uteroplacental unit
how does blood flow to the organs change during pregancy
give an example
increased
kidneys - increased by 60-80% above non-pregnant state
warm, red hands and feet
increased risk of nose bleeds, sensation of stuffiness/congestion due to increased blood flow to nasal mucosa
how does cardiac output change during pregnancy
increased as SV is increased
CO = SV X HR
CO increases by ~30-50% by the end of 2nd trimester
people who cannot increase CO (e.g. aortic stenosis) are at risk
how does HR change during pregnancy
increases
at term ~10-20 beats higher than non-pregnant value
sinus tachycardia isn’t uncommon
other pathologies causing tachycardia (hypovolaemia, pulmonary embolus, sepsis) should be considered depending on clinical context
oxygen consumption during pregnancy
increases by 20-30% at term
myocardium has to work harder therefore increased oxygen requirements
pregnancy can trigger ischaemic heart disease and MI in those w/ coronary artery disease (older, diabetic, smoker)
why can you never lie a pregnant patient flat
they will lose 25% of their cardiac output and faint
due to vena caval compression by pregnant uterus
in what position must a pregnant patient be resucitated in the event of maternal collapse/cardiac arrest
on a left lateral tilt or with the uterus manually displaced
you will not be able resucitate any person with a gravid uterus who is lying flat due to the reduction in CO
intrapartum CV changes
autotransfusion of contractions - with every contraction another (up to) 500ml is dumped into the circulation
pain - increases circulating catecholamines and increases HR, BP and CO
increase in CO during labour
can increase by a further 10% and immediately after delivery up to 80% above the already increased CO of pregnancy - due to lack of uteroplacental unit to be supplied and also immediate relief of IVC compression
post-partum CV changes
most return to normal by 3mths after delivery
3 days - blood volume decreased by 10%
3-7 days - BP initially falls then increases again
6wks - BP returns to pre-pregnancy levels
systemic vascular resistance begins to increase again over first 2wks, HR falls to prepregnancy levels
respiratory changes during pregnancy
increased oxygen requirements
increased volume of air and gas exchange with each breath - increases oxygen availability and CO2 removal in mother and foetus
changes to tidal volume during pregnancy
increases
40-50% increase in minute ventilation
changes in resp rate during pregnancy
increases
can be percieved as SOB
hyperventilation in pregnancy
relative hyperventilation
PCO2 levels are lower in pregnancy
healthy pregnant person is in a state of compensated respiratory alkalosis
changes in the chest during pregnancy
enlarging uterus pushes the diaphragm up up to 4cm
increased diameter of lower thorax by 2cm - splaying of lower ribs
changes in functional residual capacity during pregnancy
decreases ~20-30%
further reduced by supine position
asthma and pregnancy
improves in some cases
due to the bronchodilator effect of progesterone
Hb at 28wks
at 28wks a Hb of 105g/L or above is considered normal
non-pregnant range 120-160
this is the physiological anaemia of pregnancy
plasma volume and pregnancy
increases proportionate to birthweight
relative decrease in platelet count due to this - remains in normal limits for the non-pregnant patient
changes in iron levels during pregnancy
2-3x increase in requirements
mainly for use by foetus as well as increasing red cell mass
what is the most common haematological abnormality of pregnancy
iron deficiency anaemia
more common in twin/multiple pregnancies
also associated with intrauterine growth restriction
why are some women iron deficient going into pregnancy
menorrhagia
inadequate diet
previous recent pregnancies
what contributes to iron deficiency postnatally
post partum haemorrhage
2-5% of deliveries
folate requirements during pregnancy
increase 10-20x during pregnancy
2nd most common cause of pregnancy anaemia
serum levels of folate are lower in pregnancy but liver levels are maintained
changes in WCC during pregnancy
increase - overall WCC and neutrophil
WCC up to 16x109/L is normal
changes in coagulation during pregnancy
hypercoagulable state
factors which promote clotting increase, factors which prevent decrease
what clotting factors increase during pregnancy
VII, IX, X
fibrinogen
which anti-clotting factors decrease during pregnancy
protein S and C
anti-thrombin 3
fibrinolytic activity decreases
DVT risk and pregnancy
increased risk
also increased by venodilation and reduced venous return - increased venous stasis in lower limbs
pulmonary embolus and pregnancy
one of the main causes of direct maternal mortality in UK
6-15 people killed p/a in pregnancy or puerperium
pregnancy increases risk of thromboembolism by 6x
when do changes in coagulation occur
from very early in pregnancy
can persist up to 6wks after delivery
1/2 of all clots associated with the antenatal period occur in first 15wks
why does the urinary system significantly dilate during pregnancy
relaxation of smooth muscle of ureter - caused by progesterone
mechanical compression of the growing uterus
hydronephrosis and pregnancy
physiological hydronephrosis can be seen
usually more pronounced on the R side
changes in renal blood flow during pregnancy
increase in circulating blood vol and reduction in systemic vascular resistance
increase in renal plasma flow by up to 60-80% in 2nd trimester
settles to 50% increase through 3rd trimester
GFR and creatinine clearance during pregnancy
increase by ~50%
normal levels of urea and creatinine are much lower during pregnancy
changes in excretion and secretion in the kidneys during pregnancy
excrete more protein
retain more sodium (and water)
increased secretion of vit D, renin and erythropoetin
haematuria in pregnancy
microscopic haematuria is more common
if there is no proteinuria, no infection and renal US and function is normal - likely due to bleeding from the small vessels in the dilated renal function
glycosuria is also common
UTI in pregnancy
more common
should be treated w/ abx safe in pregnancy promptly
kidney disease and pregnancy
any underlying kidney disease is likely to worsen during pregnancy
due to additional work being done by the renal system
