LC Exam 2: Maternal Physiology and Pregnancy Flashcards
Total body water and pregnancy
Increased from 6.5 to 8L (2kg)
Includes expanded plasma, RBC, extra/intracellular
Preg= chronic overload state
Normal weight gain in pregnancy
1lb/wk for under/nml BMI
.5lb/wk for overweight/obese
Osmoregulation
AVP secretion increased, but inactivated by placenta
Water retention>Na retention
Net sodium loss (some from RAAS activation)
Cardio markers
RAAS elevated (5x) ANP, BNP also elevated
CV changes to blood volume
Plasma volume increased 50%
RBC mass increased 30%
Therefore dilutional anemia (Hct 32-36%)
CV changes in BP
Decline until 22 weeks, then normalization
Progesterone effect on smooth muscles and increased NO
Effect of decreased vascular resistance
HTN = >140/90
CV heart physiology changes
Increased CO (mostly SV, some HR in 3rd tri, 10 bpm)
Hypertrophy of ventricle
Increased preload, decreased afterload
Decreased CO? IVC compression by uterus -> roll
Reorganization of blood flow
No change in brain, liver, kidney
Increased perfusion to breast, skin, uterus
Uterus 2% to 15%
IVC compression can lead to edema, hemorrhoids, DVT risk
Cardio physical exam
Normal sinus
PMI is displaced left (uterus size) (left axis deviation)
Systolic ejection murmurs (LSB)
Diastolic murmur is abnormal
S3 common
Increased PVCs, some ST segment changes
Arrhythmias common (also heart closer to chest wall, easier to notice)
CXR changes
Heart size ratio unchanged
Left heart border more straight
Heart is more horizontal
Prominent pulmonary vasculature
Pulmonary edema hypothesis
Increased colloid oncotic pressure
No change in wedge pressure
More tendency to develop edema
Cardiac changes in labor and postpartum
Straining: valsalva decreases return, reflex brady, sympt discharge, maintained CO
Relax: increased return, increased MAP, reflex brady
HR relax
Valve disease in pregnancy
Regurg better tolerated then stenosis
Decrease in heart fxn (progression to HF and CHF possible)
Aortic stenosis: fixed CO, can’t increase with preg (orthostatic with increased HR)
Pulmonary changes
Rate unchanged, VC unchanged TV increases (prog effect on CO2 sensors) Decreased RV, decreased TLC FEV1 and FVC unchanged (as does ratio) PaCO2 decreases (27-32mmHg, nml 40- too high in preg) PaO2 increases pH unchanged/increases - bicarb loss HCO3 decreases
Mechanical pulmonary changes
Chest size increases
Breathing becomes more diaphragmatic (pushed up but excursion increases)
Pregnancy gas exchange
Primary respiratory alkalosis with compensatory metabolic acidosis
Less buffer available -> DKA faster with GDM
Asthma in pregnancy
May improve with increased cortisol
Keep pO2 WNL
The common therapies are still safe (beta agonists and steroids)
Kidneys during pregnancy
Enlarged organ
Hydronephrosis - right side more than left
Due to both mechanical compression and progesterone relaxation
Resolves by 6 weeks post partum
Increased pyelo risk -> more stasis (progesterone)
Kidney physiology
Increased GFR
Increased renal plasma flow (more then GFR)
Via NO increase (progesterone)
Relative hyponatremia
Chronic renal insufficency
Associated with adverse outcomes
Try and plan and get off dialysis prior to preg
Transplant if possible
Platelets
Also diluted
15% 100-150k (116k suggested as cutoff)
Immune system
WBC increases over course
1st tri: 8000
2/3rd tri: 8500 (up to 12,000)
Coagulation
Increase in most factors (decrease hemorrhage) Increased risk DVT/PE (5-6x), L>R XI and XIII decline Protein C = constant, ATIII constant Protein S = shrinks
DVT/PE treatment/prophylaxis
LMW is gold standard (switch to unfrac at 36 wks) Avoid coumadin (contraindicated) Postpartum: coumadin vs. heparin
GI changes
Increased saliva production (no change in carries)
Decreased tone/motility (progesterone)
Decreased risk of PUD
Increased GE reflux (prog relaxation)
Early saiety in 3rd
Appendix rises
Increased portal venous pressure (hemorrhoids)
Increased caloric intake during preg
1st: 200cal/day
2/3rd: 300 cal/day
Gallbladder changes
Increased residual volume
Decreased motility
Increased risk of stone
Tx: low fat diet and elective ectomy (if mid-trimester, better outcomes)
Liver changes
Spider angioma, palmar erythemia all normal (increased E2, “glow”)
Decreased albumin/protein (hemodilution)
Elevated alk phos (placental production)
Cholestasis (most common, jaundice, can lead to malabsorbtion of fat -> vit K def)
Skin changes
Hyperpigmentation (hCG stimluation of MSH)
Increased blood flow to skin
Gum hyperemia
5 important pregnancy hormones
hCG hPL hPGH Progesterone Estrogen
Iodine requirements in pregnancy
Increase
PTH-rp and pregnancy
Produced by placenta, decidua, fetal parathyroids, and mammary glands
Regulates Ca2+ transport
Increased 1,25OH x2
3 steroid hormones from placents
Progesterone
Estrogen
1,25OH Vit D
Levels: maternal»»fetal
Maternal system sees effect more than fetus
Progesterone secretion maintained by:
Main, important action
Corpus luteum up to ~8-10weeks
Placenta takes over after
Prevent preterm labor
(progesterone antagonists given as abortive tx)
a subunit of ßhCG is same as
ß subunit is similar to
FSH
LH
TSH (increased T4, decrease TSH early in preg)
ß is most similar to LH (more LH activity)
ßhCG levels
Produced 8 days after ovulation
Doubles q 48 hours for first 5-6 weeks
Peaks at 10-12 weeks (peak of n/v, maintains CL)
t1/2 = 24-36 hours
Human placental lactogen (hPL)
Secreted by synctioTB
Similar to GH and PRL (more PRL)
Made increasing amounts in pregnancy, very high at end of pregnancy
Increases insulin resistance, change to FFA metabolism
Also stimulates insulin secretion
Human placental growth hormone (hPGH)
Secreted by synctioTB
Similar to GH (not regulated by GHRH)
Causes insulin resistance
Causes decrease in pit GH secretion
Insulin resistance in pregnancy mediated by
hPL
hPGH
TNF-a (increases with preg)
Adiponectin (decreases with preg)
Progesterone
LDL receptors on placenta LDL required for progesterone synth. Promotes deciuda formation Inhibits uterine contraction Promotes Th2 response and suppress Th1 response Can actually improve autoimmunity d/o Lobular development in breast Lots of relaxant effects
Estriol
Only seen in pregnancy
Maternal cholesterol, placental progesterone, fetal DHEAS (adrenal), fetal 16-OH DHEAS (liver), placental estriol to maternal circulation
Aromatase in placenta
DHEA to E2 plus Estrone
Even in PCOS, CAH etc -> low low chance of excess virulization of fetus
Estrogen
Increased production
Produced by placenta due to aromatase (DHEAS)
Hypercoaguable state
Induces lactrotrophs (PRL, don’t give E2 with trouble feeding)
Increases blood flow, volume
Increased TG synth. (acute pan risk)
Increased pit size (Sheehan’s risk)
Insulin changes of normal pregnancy/GDM
Can reveal LADA (thin women with GDM, think LADA)
Insulin sensitivity in 1st tri, risk for night hypogly
Insulin resistance in 2nd/3rd with hPL, hPGH, TNF-a and adiponectin
GDM is risk factor for T2DM later on
OGTT in pregnancy
Normal pregnancy have normal BG but slightly higher post-prandial (due to resistance)
GDM have much higher BG levels
Why do obese women give birth to larger babies?
BG are on average higher than normal, but not GDM high
Trigly also high early and late in preg
Late -> more E2 -> more acute pan risk
Postpartum management of GDM
50% risk T2DM in 20 yrs
OGTT 6-12 weeks PP to dx or stratify risk
Contraception to prevent future preg
Breast feeding decreases T2DM risk
Neonatal GDM risk after birth
LGA, shoulder dystocia Infant RDS Hypoglycemia (mom sugar cross, high baby insulin, mom sugar gone after delivery, baby insulin still high) Hyperbili Polycythemic (outgrow own blood supply)
OGTT doesn’t help predict infant mortality (only maternal T2DM risk)
Risk factors for childhood obesity
Maternal glucose status is big but also: Maternal BMI LGA Lipids, dietary fat Rate of weight gain 0-6 months Feeding most (breast feeding is protective)
Thyroid function in pregnancy
ßhCG has TSH activity: increases T4
E2 increases binding globulin (TBG -> increases T4)
Higher T4 suppresses normal TSH
Thyroid stuff that crosses placenta
Anti-thyroid drugs cross well (make sure REAL)
TSH receptor ab (Grave’s) cross well
T4 crosses okay
Postpartum thyroiditis
Destruction of gland Histologically looks like Hashimoto's Transient increase in T4 (from cell breakdown) Risk of recurrence in future pregnancies Monitor for chronic hypothyroid Tx. transient increase with ß-blocker Tx. hypothyroid and re-evaluate in year
