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
bladder changes in pregnancy
- upward displacement
- flattening
- urinary frequency
- mechanical + hormonal
- increased bladder capacity by ~1 L
normal renal/urinary lab changes in preg
- low serum Cr (threshold of suspicion for disease also lower)
- more rapid drug ecertion
- glycosuria
- asymptomatic bacteriuria
- – strep B can be problem during cb
GI changes in pregnancy
gastric reflux more likely
- delayed gastric emptying
- relaxation of lower esophageal sphincter
- increase in gastric acid
constipation more likely
- slower transit
also
- stomach displaced upward
- increased mucus
gallbladder changes in pregnancy
stasis –> gallstones
- progesterone inhibits contractions
- decreased contractility = slow emptying
WBC changes in preg
pre-preg ~4500
preg ~5000-12000
labor ~20000-25000
predominant rise in PMNs
platelet and clotting changes in preg
VTE risk 6x
platelets
- increased production
- increased consumption
- sometimes a fall in 3rd tri d/t increase in peripheral consumption
clotting factors
- increase
- fibrinogen, V, VIII, IX, X –> thrombin
- d/t estrogen
- decreased fibrinolysis, protein S activity
venous stasis and deep vein capacitance also increase VTE risk
skin changes pregnancy
- +blood flow
- +pigmentation
- melasma
- darker nevi (rapid changes –> excision)
- less hair loss during preg
- more hair loss pp, regrowth by 6-12 mo
breast changes pregnancy
early
- tenderness
- tingling
- heavyness
- enlargement d/t
- – vascular engorgement
- – estrogen –> ductal growth
- – progesterone –> alveolar hypertrophy
later
- enlargement and pigmentation of areollae
- colostrum late in preg
- milk production
- – estrogen
- – progesterone
- – prolactin
- – hPL
- – cortisol
- – insulin
lactation
- drop in E and P pp
- progesterone inhibits lactation
- maternal prolactin decreases pp, but not as much as progesterone –> lactation
- pulsatile prolactin d/t suckling –> milk
“let down”
- suckling –> oxytocin –> release by myoepithelial cells
thyroid changes in preg
- increased
- alpha hCG = TSH
- thyroid enlargement d/t hyperplasia and vascularity
- TBG (binding globulin) +2-3x d/t estrogen
clinically:
- don’t check total T4 or T3, check ratio FT3/FT4
- low TSH common in 1st tri
- transient hyper-T4 in first tri
metabolism and nutritional requirement in preg
- increased metabolic demands
- 300-400 cal/day in 2nd and 3rd tri
- protein recommendations increase
- carb recommendations increase
- no rec for fat d/t optimal not known
weight gain rec in preg
BMI <18.5
- total +30-40 lb
- 1-4 lb 1st tri
- 1-1.5lb/wk 2nd and 3rd
BMI 18.5-24.9
- total +25-35 lb
- 1-4 lb 1st tri
- 1lb/wk 2nd and 3rd
BMI 25-29.9
- total +15-25 lb
- 1-4 lb 1st tri
- 0.5 lb/wk 2nd and 3rd
BMI ≥30
- total +10-20 lb
- 1-4 lb 1st tri
- > 0.5 lb/wk therafter
miscarriage/spontaneous abortion vs. stillbirth
SAB <20wk or fetus <500g
stillbirth thereafter
G&P
gravida = number of pregnancies, including the current one
para = delivery after 20 wk, abortion prior to 20 wk, living children
SAB incidence
15-20%
80% of which <12 wk
categories of SAB
- threatened
- inevitable
- complete
- incomplete
- missed
- septic
- anembryonic/blighted ovum
threatened SAB
- bleeding
- closed cervical os
- no tissue passage
- watch and wait
- bedrest no longer indicated as no clinical benefit
inevitable SAB
- bleeding or leaking fluids
- dilated cervical os
- imminent fetal loss
- POC not yet passed
- ± fever, pain
- may require medical or surgical intervention
complete SAB
- all POC (products of conception) expelled
- hx of heavy vaginal bleeding
- closed cervical os (b/c already closed again)
- generally no further treatment or f/u needed
incomplete SAB
- some POC expelled
- bleeding, cramping
- open cervical os
- watch and wait
- may need medical or surgical mgmt