Physiology 2 Flashcards
Weeks of full pregnancy?
40 from first day LMP
Weeks for viability of baby?
~24
Weeks for preterm baby?
viable - 37 weeks
Prenatal Care of?
- mother
- fetus
- family
Initial Visit for mother?
- screening history, physical, labs
- identification of specific “high risk” factors
- anticipate problems
Chromosome assessment
-age based
Early Term
37-38
Term
39-40
Late Term
41
Post Term
42
-no one goes this far anymore
Progressive Monitoring of Pregnant Mother
- weight gain
- bp
- Rh, diabetes, anemia, STD, group B strep carrier
- plan for delivery
Nutrition of Pregnant Mom
- weight gain - plus
- obesity is a form of malnutrition
- essential amino acids (9)
Blood pressure with Pregnant Mom
- Pre-existing: medications-contraindicated ACE inhibitors, 50% congential malformation if organogenesis exposure
- Hypertension of pregnancy:
- gestational
- pre-eclampsia
Pre-eclampsia
- HTN, proteinuria, attributable to being pregnant
- natural history leads to death
- just plain strange syndrome: no good animal models
- one of the major complications of pregnancy
- eclampsia is convulsions
Rh
- rhesus (monkey) D antigen
- prior pregnancy event
- mom Rh negative, baby positive, possible sensitize mon, develops antibodies “rejects next pregnancy”
- Solution: coat the fetal red cells which may contain Rh antigens using IgG so mom doesn’t “see” antigen
Diabetes in Pregnancy
- Pre-existing
- Gestational (45-50% dev overt DM later in life)
- Diet Controlled
- Insulin-Dependent (body can’t make type 1, insentitive type 2)
- oral hypoglycemic
- high risk: prior DM in pregnancy, multiple gestation, AMA, obese
Eclampsia
convulsions
hCG - alpha structure
- similar to TSH
- similar to insulin
Fetus Monotering
- gestational age
- one or more
- survey anatomic structural at 18-20 weeks
- routine growth
- well-being
- movement
Ultrasound
- structure (also where and how many)
- blood flow
- amniotic fluid
Fetal Heart Rate Monitoring
- strict criteria 110-160 BPM baseline rate
- heart rate “accelerations”
- heart rate “decelerations”
Family Issues with Pregnancy
- mixing medicinve and sociology
- finances
- work
- other children
- delivery planning
Onset of Labor
- Contractions
- Bleeding
- Rupture of membranes “water breaks”
Labor
- regular, phasic contractions sufficient to cause progressive dilation of the cervix
1. Latent Phase - “pre labor” <4cm
2. Active Phase - 1st 4-10cm
3. Pushing - 2nd
4. Delivery placenta 3rd
Viability
-ability to live outside the uterus
Premature
-fetus is premature, different that preterm
What % of pregnancies are normal?
75% "retrospective diagnosis" -not counting repeat C/S -Complications of pregnancy: infection, preterm labor, pre-eclampsia, prior C/S, not vertex
Contraction
- start
- peak
- end
Duration of Latent
no limit
Duration of Active
-Friedman curve, actually 1-2cm/hr
Duration of 2nd stage
-3 hr primip or 2 hr multip
Duration of 3rd stage
-1 hour
Vaginal Birth
-regular, normal, usual
Delivery of Placenta
- gentle traction: do not avulse cord
- is it intact?
- 3 vessels
- bleeding?
Assess for Damage
- cervical laceration
- vaginal wall laceration
- perineum laceration
- vulvar laceration
Perineum Lacerations
1st degree-skin only
2nd-defect of underlying tissue but not through anal sphincter (must repair)
3rd-into or through sphincter (repair)
4th-defect of rectum (repair)
Assisted Vaginal Delivery
- forceps
- vacuum (no only if have to, or if don’t want mom to push)
Cesarean Delivery
- abdominal delivery
- vaginal bypass operation
- C/S, CSD
- Tocolytic (toco-childbirth cutting, really means stopping preterm birth)
Cesarean Rate
- the C/S rate is too high or too low
- US: low 30% (20% for primigravidas)
- Puerto Rico is 70%
Vaginal Birth after Cesarean Section
- uterine scar: ruptured uterus with subsequent labor
- repeat C/S
- if many more children are desired, trial of labor
- vaginal birth after C/S
Risk of C/S
- increased bleeding
- increased risk of infection
- increased risk of intraabdominal scarring
- increased risk of uterine rupture with each additional C/S
- Increased risk of placenta accreta, next pregnancy
Maternal Mortality: Statistics
- 250,000-343,000 deaths worldwide
- 99% in economically disadvantaged countries
- nearly linearly associated with illiteracy rate, education, poverty
- morbidity is 20x mortality
Maternal Mortality
-death occurring during pregnancy, or within 6 weeks of delivery, excluding accidents or if the pregnancy is incidental to cause of death
MMR
-maternal mortality ratio: # deaths/100,000 live births in one year
(ratio)
Maternal Mortality Rate
deaths/ # women of reproductive age
How many maternal deaths in US are preventabe?
50% - 27%
Problems that lead to ectopic pregnancy?
- damage to cilia
2. blind pouch
Why recient rise in mortality?
- obesity
- immigration
- increased C/S rates
- IVF: twins
- High unintended pregnancy
- no pre pregnancy counseling
- domestic abuse rates are high in US
Racial Disparity in Pregnancy
- african american: white 4:1
- education not independent risk factor
- income not independent risk factor
Extremely Preterm
<28 weeks
Very Preterm
28 to <32 weeks
Moderate to late Preterm
32 to <37 weeks
Cardiovascular Adaptation During Pregnancy
#1-systemic vascular resistance goes down (dec. 20-25% in early pregnancy, reached by 5 weeks) #2-blood volume goes up 30%, need to supply baby -bp & heme decrease
What group of cells remodel the spiral arteries?
-cytrtrophoblasts (extravascular trophoblast)
Remodeled Vessels are??
high-flow
low-resistance
When does remodlin start?
at 4 weeks of pregnancy
Invasive Trophoblasts
- uterine spiral artery containing maternal blood
- maternal endometrium has become decidualized meaning that the stromal cells have been transformed into large pail cells
- infiltrating b/w these decidual cells are trophoblasts
hCG levels level off when?
-at 20 weeks (baby grows by deposition of fat)
What causes total vascular resistance to decrease?
-reduced vasomotor tone and remodelling of resistance-sized arteries (because of remodin & ADAM 12)
Women with preeclampsia have higher and lower what?
Higher: conc. of sVEGRF-1 and sENG
Lower: conc. P1GF
-have imbalance of angiogenic/antioangiogenic factors
Regulation of Cardiac Output during Pregnancy?
- maternal vasodilation
- decreased ventricular afterload (1st trimester)
- increase in cardiac output & relative arterial underfilling
- increased preload
- decreased afterload
- increased compliance
Physiologic anemia of pregnancy?
-increase in plasma volume is faster than increase in erythrocyte volume (give iron)
Timing of Plasma Volume change?
- happens in 4-8 weeks
- returns to normal 6 weeks after delivery
What happens if plasma volume doesn’t increase enough?
-related to not enough fetal growth
Does the heart change in pregnancy?
- yes, ventricular remodeling
- apical four chamber views showing the normal heart remodelling with eccentric hypertrophy in a normal third trimester pregnant women
- increased myocyte volume without fibrosis, increased heart elasticity to comply with increased volume
- increased injection fraction, stroke volume, cardiac output
Renal Adaptation in Pregnancy
- GFR increases by up to 50% above baseline (b/c elevations in cardiac output & kidney blood flow)
- decrease in serum creatine concentration (0.4mg/dL)-normal levels 0.9 may indicate kidney disease
- hydronephrosis (more on right)
Why do pregnant women have hydronephrosis?
-progesterone-induced ureteral smooth muscle relaxation and ureteral compression secondary to the enlarging fetus results in dilatation of the urinary collecting system
Respiratory System in Pregnancy
-uterus enlarges, diaphragm is elevated (4cm), doesn’t impede movement
-rib cage is displaced upward & widens, increasing the lower throacic diameter by 2cm and thoracic circumference by 6cm
-chest circumference expands 5-7cm
-subcostal angle increases from 68-103 deg
-respiratory muscle function is not affected
-abdominal muscles have less tone, less active
MORE DIAPHRAGMATIC
In pregnancy, what happens to dead volume?
-increases to relaxation of the musculature of the conducting airways
Pregnancy: Tidal Volume
-increases gradually (35-50%) as pregnancy progresses
Pregnancy: Total Lung Capacity
-reduced (4-5%) by elevation of the diaphragm
Pregnancy: Functional Residual Capacity, Residual Volume, Respiratory Reserve Volume
-dec. by 20%
Pregnancy: Residual Volume, Tidal Volume
Residual Volume smaller & Tidal Volume Larger caused by increased alveolar ventilation (about 65%) during pregnancy
Pregnancy: Inspiratory Capacity
-increases 5-10%
Pregnancy: Alveolar Oxygen Tension
-in normal limits, lowers maternal blood CO2 tension
Maternal Hyperventilation
-considered a protective measure that prevents that fetus from the exposure to excessive levels of CO2
Gas Exchange in Pregnancy
-hyperventilation leads to decreased PCO2
-increases CO2 gradient b/w fetus and mother
-chronic respiratory alkalosis
-compensatory metabolic acidosis
-20-40% increased in maternal oxygen consumption
-normal arterial blood gas values pH-7.4-7.45
PCO2 = 28-32 PO2=101-106 HCO3=18-21
Hormone Changes in Pregnancy
- pregnancy increases estrogen/progesterone
- increase prolactin
- decrease pituitary growth hormone b/c placental GH takes over
- adiponecin decreases
Pregnancy looks hormonally similar to?
Obesity
How is pregnancy like obesity?
- insulin resistance
- leptin resistance (need increased fat content for babies brain), made by placents (10x)
- high cortisol level
Does bacteria change in pregnancy?
-yes, causes increased insulin resistance
Pregnancy HPA axis?
- placental CRH stimulates both the maternal pituitary and adrenal, leading to increased cortisol producing
- rising cortisol stimulates placental CRH production
Passage of cortisol through placenta?
- partially inhibited by placental HSD2
- if to much gets to baby, bad effects
What happens if mother has stress or 11beta-HSDw is decreased?
-baby gets more cortisol in its blood
Mechanisms of Materno-Fetal Transfer
- transported intact
- partially consumed by placenta
- metabolized by placenta (cortisol)
- not transported
What are stem cells of the placenta?
-cytotropyoblasts
Endocytosis/Exocytosis
-uptake form maternal blood by endocytosis transport across cytosol via vesicular transport released into fetal circulation via exocytosis (immunoglobulins)
Lipophillic Diffusion
-hydrophobic molecules soluble in plasma membrane (respiratory gases)
Paracellular Diffusion
-hydorphillic molecules exchanged via water filled channels/pores, driven by electrochemical driving forces (small solutes, sodium, calcium, K)
Protein Mediated Transport
-hydrophillic molecules, mediated via specific proteins in maternal and fetal facing plasma membranes (ions, amino acids, glucose)
What is the primary barrier for transfer of nutrients from mother to fetus?
-syncytiotrophoblast
What type of transports are increased towards the end of pregnancy?
-fat transporters
-What type of fatty acids does placental tissue preferentially take up?
-long-chain polyunsaturated fatty acids (LC-PUFAs)
