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Reproductive > Physiology 2 > Flashcards

Physiology 2 Flashcards

1
Q

Weeks of full pregnancy?

A

40 from first day LMP

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2
Q

Weeks for viability of baby?

A

~24

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3
Q

Weeks for preterm baby?

A

viable - 37 weeks

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4
Q

Prenatal Care of?

A
  • mother
  • fetus
  • family
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5
Q

Initial Visit for mother?

A
  • screening history, physical, labs
  • identification of specific “high risk” factors
  • anticipate problems
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6
Q

Chromosome assessment

A

-age based

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7
Q

Early Term

A

37-38

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8
Q

Term

A

39-40

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9
Q

Late Term

A

41

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10
Q

Post Term

A

42

-no one goes this far anymore

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11
Q

Progressive Monitoring of Pregnant Mother

A
  • weight gain
  • bp
  • Rh, diabetes, anemia, STD, group B strep carrier
  • plan for delivery
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12
Q

Nutrition of Pregnant Mom

A
  • weight gain - plus
  • obesity is a form of malnutrition
  • essential amino acids (9)
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13
Q

Blood pressure with Pregnant Mom

A
  1. Pre-existing: medications-contraindicated ACE inhibitors, 50% congential malformation if organogenesis exposure
  2. Hypertension of pregnancy:
    - gestational
    - pre-eclampsia
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14
Q

Pre-eclampsia

A
  • 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
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15
Q

Rh

A
  • 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
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16
Q

Diabetes in Pregnancy

A
  1. Pre-existing
  2. Gestational (45-50% dev overt DM later in life)
  3. Diet Controlled
  4. Insulin-Dependent (body can’t make type 1, insentitive type 2)
  5. oral hypoglycemic
  6. high risk: prior DM in pregnancy, multiple gestation, AMA, obese
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17
Q

Eclampsia

A

convulsions

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18
Q

hCG - alpha structure

A
  • similar to TSH

- similar to insulin

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19
Q

Fetus Monotering

A
  • gestational age
  • one or more
  • survey anatomic structural at 18-20 weeks
  • routine growth
  • well-being
  • movement
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20
Q

Ultrasound

A
  1. structure (also where and how many)
  2. blood flow
  3. amniotic fluid
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21
Q

Fetal Heart Rate Monitoring

A
  • strict criteria 110-160 BPM baseline rate
  • heart rate “accelerations”
  • heart rate “decelerations”
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22
Q

Family Issues with Pregnancy

A
  • mixing medicinve and sociology
  • finances
  • work
  • other children
  • delivery planning
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23
Q

Onset of Labor

A
  1. Contractions
  2. Bleeding
  3. Rupture of membranes “water breaks”
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24
Q

Labor

A
  • 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
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25
Q

Viability

A

-ability to live outside the uterus

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26
Q

Premature

A

-fetus is premature, different that preterm

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27
Q

What % of pregnancies are normal?

A 
75%
"retrospective diagnosis"
-not counting repeat C/S
-Complications of pregnancy:
  infection, preterm labor, pre-eclampsia, prior C/S, not vertex
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28
Q

Contraction

A
  1. start
  2. peak
  3. end
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29
Q

Duration of Latent

A

no limit

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30
Q

Duration of Active

A

-Friedman curve, actually 1-2cm/hr

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31
Q

Duration of 2nd stage

A

-3 hr primip or 2 hr multip

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32
Q

Duration of 3rd stage

A

-1 hour

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33
Q

Vaginal Birth

A

-regular, normal, usual

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34
Q

Delivery of Placenta

A
  • gentle traction: do not avulse cord
  • is it intact?
  • 3 vessels
  • bleeding?
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35
Q

Assess for Damage

A
  • cervical laceration
  • vaginal wall laceration
  • perineum laceration
  • vulvar laceration
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36
Q

Perineum Lacerations

A

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)

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37
Q

Assisted Vaginal Delivery

A
  • forceps

- vacuum (no only if have to, or if don’t want mom to push)

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38
Q

Cesarean Delivery

A
  • abdominal delivery
  • vaginal bypass operation
  • C/S, CSD
  • Tocolytic (toco-childbirth cutting, really means stopping preterm birth)
39
Q

Cesarean Rate

A
  • the C/S rate is too high or too low
  • US: low 30% (20% for primigravidas)
  • Puerto Rico is 70%
40
Q

Vaginal Birth after Cesarean Section

A
  • uterine scar: ruptured uterus with subsequent labor
  • repeat C/S
  • if many more children are desired, trial of labor
  • vaginal birth after C/S
41
Q

Risk of C/S

A
  1. increased bleeding
  2. increased risk of infection
  3. increased risk of intraabdominal scarring
  4. increased risk of uterine rupture with each additional C/S
  5. Increased risk of placenta accreta, next pregnancy
42
Q

Maternal Mortality: Statistics

A
  • 250,000-343,000 deaths worldwide
  • 99% in economically disadvantaged countries
  • nearly linearly associated with illiteracy rate, education, poverty
  • morbidity is 20x mortality
43
Q

Maternal Mortality

A

-death occurring during pregnancy, or within 6 weeks of delivery, excluding accidents or if the pregnancy is incidental to cause of death

44
Q

MMR

A

-maternal mortality ratio: # deaths/100,000 live births in one year
(ratio)

45
Q

Maternal Mortality Rate

A

deaths/ # women of reproductive age

46
Q

How many maternal deaths in US are preventabe?

A

50% - 27%

47
Q

Problems that lead to ectopic pregnancy?

A
  1. damage to cilia

2. blind pouch

48
Q

Why recient rise in mortality?

A
  • obesity
  • immigration
  • increased C/S rates
  • IVF: twins
  • High unintended pregnancy
  • no pre pregnancy counseling
  • domestic abuse rates are high in US
49
Q

Racial Disparity in Pregnancy

A
  • african american: white 4:1
  • education not independent risk factor
  • income not independent risk factor
50
Q

Extremely Preterm

A

<28 weeks

51
Q

Very Preterm

A

28 to <32 weeks

52
Q

Moderate to late Preterm

A

32 to <37 weeks

53
Q

Cardiovascular Adaptation During Pregnancy

A 
#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
54
Q

What group of cells remodel the spiral arteries?

A

-cytrtrophoblasts (extravascular trophoblast)

55
Q

Remodeled Vessels are??

A

high-flow

low-resistance

56
Q

When does remodlin start?

A

at 4 weeks of pregnancy

57
Q

Invasive Trophoblasts

A
  • 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
58
Q

hCG levels level off when?

A

-at 20 weeks (baby grows by deposition of fat)

59
Q

What causes total vascular resistance to decrease?

A

-reduced vasomotor tone and remodelling of resistance-sized arteries (because of remodin & ADAM 12)

60
Q

Women with preeclampsia have higher and lower what?

A

Higher: conc. of sVEGRF-1 and sENG
Lower: conc. P1GF
-have imbalance of angiogenic/antioangiogenic factors

61
Q

Regulation of Cardiac Output during Pregnancy?

A
  • maternal vasodilation
  • decreased ventricular afterload (1st trimester)
  • increase in cardiac output & relative arterial underfilling
  • increased preload
  • decreased afterload
  • increased compliance
62
Q

Physiologic anemia of pregnancy?

A

-increase in plasma volume is faster than increase in erythrocyte volume (give iron)

63
Q

Timing of Plasma Volume change?

A
  • happens in 4-8 weeks

- returns to normal 6 weeks after delivery

64
Q

What happens if plasma volume doesn’t increase enough?

A

-related to not enough fetal growth

65
Q

Does the heart change in pregnancy?

A
  • 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
66
Q

Renal Adaptation in Pregnancy

A
  • 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)
67
Q

Why do pregnant women have hydronephrosis?

A

-progesterone-induced ureteral smooth muscle relaxation and ureteral compression secondary to the enlarging fetus results in dilatation of the urinary collecting system

68
Q

Respiratory System in Pregnancy

A

-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

69
Q

In pregnancy, what happens to dead volume?

A

-increases to relaxation of the musculature of the conducting airways

70
Q

Pregnancy: Tidal Volume

A

-increases gradually (35-50%) as pregnancy progresses

71
Q

Pregnancy: Total Lung Capacity

A

-reduced (4-5%) by elevation of the diaphragm

72
Q

Pregnancy: Functional Residual Capacity, Residual Volume, Respiratory Reserve Volume

A

-dec. by 20%

73
Q

Pregnancy: Residual Volume, Tidal Volume

A

Residual Volume smaller & Tidal Volume Larger caused by increased alveolar ventilation (about 65%) during pregnancy

74
Q

Pregnancy: Inspiratory Capacity

A

-increases 5-10%

75
Q

Pregnancy: Alveolar Oxygen Tension

A

-in normal limits, lowers maternal blood CO2 tension

76
Q

Maternal Hyperventilation

A

-considered a protective measure that prevents that fetus from the exposure to excessive levels of CO2

77
Q

Gas Exchange in Pregnancy

A

-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

78
Q

Hormone Changes in Pregnancy

A
  • pregnancy increases estrogen/progesterone
  • increase prolactin
  • decrease pituitary growth hormone b/c placental GH takes over
  • adiponecin decreases
79
Q

Pregnancy looks hormonally similar to?

A

Obesity

80
Q

How is pregnancy like obesity?

A
  • insulin resistance
  • leptin resistance (need increased fat content for babies brain), made by placents (10x)
  • high cortisol level
81
Q

Does bacteria change in pregnancy?

A

-yes, causes increased insulin resistance

82
Q

Pregnancy HPA axis?

A
  • placental CRH stimulates both the maternal pituitary and adrenal, leading to increased cortisol producing
  • rising cortisol stimulates placental CRH production
83
Q

Passage of cortisol through placenta?

A
  • partially inhibited by placental HSD2

- if to much gets to baby, bad effects

84
Q

What happens if mother has stress or 11beta-HSDw is decreased?

A

-baby gets more cortisol in its blood

85
Q

Mechanisms of Materno-Fetal Transfer

A
  1. transported intact
  2. partially consumed by placenta
  3. metabolized by placenta (cortisol)
  4. not transported
86
Q

What are stem cells of the placenta?

A

-cytotropyoblasts

87
Q

Endocytosis/Exocytosis

A

-uptake form maternal blood by endocytosis transport across cytosol via vesicular transport released into fetal circulation via exocytosis (immunoglobulins)

88
Q

Lipophillic Diffusion

A

-hydrophobic molecules soluble in plasma membrane (respiratory gases)

89
Q

Paracellular Diffusion

A

-hydorphillic molecules exchanged via water filled channels/pores, driven by electrochemical driving forces (small solutes, sodium, calcium, K)

90
Q

Protein Mediated Transport

A

-hydrophillic molecules, mediated via specific proteins in maternal and fetal facing plasma membranes (ions, amino acids, glucose)

91
Q

What is the primary barrier for transfer of nutrients from mother to fetus?

A

-syncytiotrophoblast

92
Q

What type of transports are increased towards the end of pregnancy?

A

-fat transporters

93
Q

-What type of fatty acids does placental tissue preferentially take up?

A

-long-chain polyunsaturated fatty acids (LC-PUFAs)

Reproductive (14 decks)

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