Pregnancy pathophys Flashcards
consequences of dysfunctional early placenta dev
- prematurity
- fetal growth restriction
- stillbirth
- preeclampsia
due date calc
LMP + 280 days ~40wk
EDD often corrected based on crown-rump length in 1st tri, more accurate indication of start of pregnancy
how long conception –> implantation
1 wk
“pregnancy” starts when egg implants
trophoblast differentiation and function
b//c placenta
syncytiotrophoblasts
- produce hormones (hCG to maintain corpus lutem)
- proteases to degrade endometrium
cytotrophoblasts
- direct contact with maternal blood = uteroplacental circulation
- during invasion extravillous trophoblasts seek sPIRal arteries
- remodeling of spiral arteries
preeclampsia mx
- high bp during pregnancy
- risk of eclampsia
- d/t inadequate placental invasion during early pregnancy
mx:
- myometrial spiral arterioles undisturbed by trophoblasts = still responsive to maternal vasomotor
- impaired blood supply to placenta –> increased maternal bp
- sFLT –> endothelial dysfunction (anti-angiogenic)
signalling molecules in placentation
angiogenic:
- support formation of new blood vessels
- PIGF - placental growth factor
- VEGF
anti-angiogenic
- prevent maternal endothelial cells from resealing ends of spiral arteries
- prevent maternal blood vessels from entering fetal compartment
- prevent fetal vessels from growing out into uterus
- sFLT-1
- increased in preeclampsia
placenta accreta spectrum
excessive invasion of placenta into uterus
*hemorrhage risk
- accreta = villi attached to myometrium
- increta = villa invade myometrium
- percreta = villi invade through myometrium
placental hemorrhage ddx
- placenta accreta spectrum (accreta < increta < percreta)
- placenta previa (covering cervix)
- placental abruption (*trauma, smoking, hypertension, preeclampsia, cocaine)
fetal nutrition in pregnancy
first 10-12 weeks = diffusion/histiotrophic
then vascular circulation/hemotrophic
placental hormones
syncytiotrophoblast
- influence maternal physiology
- beta-hCG maintains corpus luteum
- progesterone synthesized de novo from cholesterol, maintains endometrium and pregnancy
- hPL ~ GH, decreases maternal insulin sensitivity and glucose
- CRH –> fetal ACTH, onset of labor
cytotrophoblast
- prevent maternal hormones from entering fetal compartment
hCG testing
- blood detection at 3 weeks (1 wk post-conception)
- urine @ 4 wk
- doubles every 48 hours in early pregnancy
- peaks at 8-10 wk
thyroid hormones in preg
alpha-hCG is identical to TSH, stimulates T3/T4 production
- T3/T4 increases throughout pregnancy and don’t fall much even after hCG has dropped
- TSH inversely proportional to hCG, initial significant dip followed by recovery as hCG peaks and drops ~8-10 wk
progesterone in pregnancy
- initially produced by corpus luteum
- then directly by placenta via de novo synthesis from cholesterol
“pro-gestation”
- immune tolerance to fetus
- hair growth
- inhibits prolactin
- increases respiration (maternal)
- smooth muscle relaxation –> vasodilation (important d/t increase in plasma volume)
- inhibits uterine contraction
sfx:
- GI: constipation, gallstones
- possible orthostatic hypotension
CVD in preg - presentation
htn ≥ 140
HR ≥ 120
crackles, S3, gallop
O2 ≤ 90%
(some or all of above)
estrogens in pregnancy
- increases across gestation
- fetal DHEAs (fetal adrenal) –> estraDIol (E2) and *esTRIol (E3)
- b/c placenta lacks 17alpha hydroxylase only DHEA pathway, no de novo synthesis
low estriol ~ poor outcome
fx
- endometrial and uterine growth
- placental angiogenesis
- breast enlargement
sfx
- nausea
- hepatic clotting factors (increased clotting)
- estriol –> contractions, labor onset
hPL
human placental lactogen similar to GH shunts resources to baby - decreases maternal insulin sensitivity - decreases maternal glucose use - increases maternal lipolysis also mammogenesis
CRH
increases fetal ACTH
involved in immunosuppression
involved in onset of labor
blood changes in pregnancy
increased blood volume by ~50%
- protection from blood loss at delivery
- circulation to baby
- starts at 6-8 wk
- possibly triggered by estrogen stim of RAAS
increased red cell mass by ~20-30%
- EPOesis d/t progesterone, hPL, prolactin
- increase iron demand
- lower blood viscosity – intervillous circulation, protect VTE
dilution anemia (more increase in blood volume than red cell mass)
CV changes in pregnancy
increase ventricular muscle mass and contractility
- dilated heart but no reduction in EF
- starts in 1st trimester
- EDV increases in late pregnancy
CO increase by ~30-50%
- most in first 8 wk
- SV declines somewhat at term
- postural - drops ~25% when supine, postural hypotension in ~8%
- distribution mainly to uterus, kidneys, breast, and skin
- no change in flow to brain, liver
SVR decreases ~35-40%
- starting as early as 5 wk
- ? why, progesterone, NO, low resistance placental circulation
BP decreases 5-10/10-15 mmHg
- ~24 wk
- affected by posture
- except in preeclampsia
CV changes intrapartum (during labor) and postpartum
further increase in CO
- E/NE rise d/t pain
- autotransfusion d/t contractions
- less affected if +epidural, left lateral position
CO increases another ~80% in first 15 min postpartum
- autotransfusion d/t contractions
- relief of aortocaval compression
CO returns to pre-labor ~1 h post-delivery
CO, SV, SVR do not return to pre-pregnancy until 12+ wk PP
PE CV findings in preg
normal:
- 3rd heart sound
- flow murmurs
- up/lateral heart displacement CXR
abnormal:
- systolic murmur >2/4
- chronic hypertension
expected but abnormal:
- decompensation of underlying CVD
respiratory changes in pregnancy
- O2 demand +20-40%
- tidal volume +40%
- minute ventilation +30-50%
- no change in RR
- decreased functional residual capacity d/t shmooshing ~20%
- less reserve but no change in VC
- no change in FEV1
why?
- progesterone is a respiratory stimulant
- increased sensitivity of medulla to CO2
acid-base changes in pregnancy
normal:
- mild respiratory alkalosis
- hyperventilation –> hypOcapnia
- facilitates CO2 fetus –> mom
- partial compensation +bicarb
abnormal:
- mild CO2 elevation PaCO2 >35 is respiratory failure
- requires intubation at that point
- e.g. acute asthma attack
renal changes in pregnancy
structure:
- larger +1-1.5cm
- dilated calyces and pelvis
- dilated ureters
- right > left d/t dextrorotation of uterus
- persists 3-4 mo PP
fx:
- flow +50-85%
- GFR +50% all in 1st tri
- vasodilation of pre and post glomerular vessels w/o change in pressure
- fall in serum creatinine
- saturation of glucose reabsorption –> glucosuria
- no hematuria
- protein loss <300mg/24 h