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Flashcards in Repro Week 2 Deck (206)
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1
Q

what two processes determine successful implantation of the fertilized egg?

A
  1. decidual reaction–> hormone dependent differentiation of the endometrium
  2. embryo (at the blastocyst stage) must acquire ability to interact with the endometrium
2
Q

at what point in the menstrual cycle is the endometrium receptive to the blastocyst?

A

only for a limited period

8-10 days after LH surge/6-7 days post-ovulation in 85% of pregnancies

this time period correlates with the highest circulating levels of progesterone

3
Q

what is the “hormone of pregnancy”?

A

progesterone

progesterone is “pro-gestation”

4
Q

where does implantation of the fertilized egg occur?

A

implantation occurs on the upper posterior wall of the uterus with the embryonic pole (the side which is in closest proximity to the inner cell mass) oriented towards the uterine epithelium

5
Q

what are the 3 stages of implantation?

A
  1. apposition–microvilli on trophoblast surface interdigitate with pinopodes on uterine epithelium
  2. adhesion–increased physical interaction
  3. invasion–blastocyst penetrates uterine epithelium
6
Q

when does decidualization of the endometrium begin?

A

during the proliferative phase of menstruation and it continues after implantation

7
Q

describe the morphological changes that occur during decidualization of the endometrium

A
  1. increase in cell size and change in shape
  2. development of intracellular organelles for protein secretion
  3. formation of intracellular junctions
8
Q

describe the functional changes that occur during decidualization of the endometrium

A
  1. prolactin and IGFBP-1 (insulin-like growth factor binding protein) secretion
  2. glycogen and lipid accumulation
9
Q

what is the decidua?

A

the endometrium in pregnancy

10
Q

what is decidualization?

A

the process by which the endometrium changes in response to progesterone

11
Q

what are the 4 regions of the decidua?

A
  1. decidua parietalis
  2. decidua capsularis
  3. decidua basalis
  4. decidua vera
12
Q

what is the decidua parietalis?

A

decidua that doesn’t include the implantation site

13
Q

what is the decidua capsularis?

A

thin capsule of endometrium covering the embryo

14
Q

what is the decidua basalis?

A

implantation site (maternal portion of the placenta)

15
Q

what is the decidua vera?

A

attenuated decidua parietalis and capsularis that becomes indistinguishable in second trimester

16
Q

where does fertilization occur?

A

in the ampulla of the fallopian tube

17
Q

what structure does the fertilized egg form first? how long does this structure persist? how many cells does it have?

A

morula

day 0-4

ball of 16-32 cells

will segregate to form inner and outer cell masses

18
Q

what structure does the zygote form after the morula? characterize its different components

A

blastocyst

inner cell mass–> embryonic pole

outer cell mass–> trophoblast

the trophoblast gives rise to the cytotrophoblast and the syncytiotrophoblast cell layers

the blastocyst cavity is the fluid filled space

19
Q

describe the human placenta

A
  1. hemochoridal –> maternal blood in direct contact with trophoblast cells
  2. discoid
20
Q

how many days post-conception does implantation begin?

A

day 6-7

syncytiotrophoblasts invade endometrium, eroding maternal tissue

21
Q

describe the development of the placenta/implantation between days 9-12 post-conception

A
  1. further advancement of syncytiotrophoblast
  2. outgrowth of columns of cytotrophoblast (primary villus columns) from the chorionic plate towards the outer edge of conceptus (embryo)
  3. cavities (lacunar spaces) appear in the syncytial trophoblast (site into which maternal blood flows to mediate nutrient exchange)
22
Q

when does villus development occur in the developing placenta?

A

days 12-17

23
Q

describe the stages of villus development in the developing placenta

A
  1. primary villi–day 12
    - inner villus cytotrophoblast and outer syncytiotrophoblast
  2. secondary villi–day 15
    - mesenchymal intrusion into primary villi
  3. tertiary villi–day 17
    - fetal capillary networks develop within villus mesenchyme
    - beginning of fetal blood supply
24
Q

at what day do advancing cytotrophoblasts reach maternal spiral arteries?

A

day 22

cytotrophoblasts at distal end of the villus columns move through the outer syncytiotrophoblasts and expand laterally to meet with cytotrophoblasts from other columns forming cytotrophoblast shell

25
Q

what is the basal plate in the developing placenta?

A

the complete cytotrophoblast shell forms the basal plate, which is the peripheral region of the placenta on the maternal side that is in contact with the uterine wall

26
Q

what are the definitive elements of the placenta that are present by day 22?

A
  1. chorionic plate from which the villi arise
  2. the villi themselves through which fetal blood will flow
  3. basal plate to which the villi are attached
  4. lacunar spaces into which maternal blood flows
27
Q

what do invasive extravillous trophoblasts (EVT) arise from? what is their purpose

A

from cytotrophoblast cells which differentiate into EVTs

these are critical for placental angiogenesis

28
Q

describe the initial vascularization of the placenta

A
  • cytotrophoblasts migrate out of villi and undergo interstitial invasion of the myometrium and endovascular invasion of maternal spiral arteries
  • endovascular trophoblast invasion results in thick walled, muscular spiral arteries being transformed into flaccid, sac like vessels which can accomodate tremendous increases in placental blood flow that occurs during pregnancy
  • failure of this process can be associated with development of preeclampsia or intrauterine growth restriction (IUGR)
29
Q

list the fetal components of the placenta

A
  1. umbilical cord
  2. amnion
  3. lacunae
  4. fetal placental vasculature
  5. chorionic plate
  6. basal plate
  7. villi
  8. cotyledon
30
Q

list the maternal components of the placenta

A
  1. decidua
  2. maternal placental vasculature (spiral arteries)
  3. intervillous space filled with maternal blood
31
Q

when does the formation of the definitive placenta occur?

A

from day 60 onwards

32
Q

describe the formation of the definitive placenta

A
  1. placenta becomes restricted to interface between fetus and decidua
  2. primary villi undergo repeated branching–> 50-60 dense “basket-like” structures
  3. basal plate expands further into the uterine stroma so that maternal spiral arteries can connect directly into the intervillous space
  4. formation of 10-40 cotyledons
33
Q

what are cotyledons?

A

partial septa arising from the basal plate into the intervillus space

visible from the maternal side of the placenta

34
Q

what is the functional unit of maternal-fetal exchange?

A

placental villi

35
Q

how do the placental villi change throughout gestation?

A

throughout gestation the villi become incerasingly branched from stem villi to intermediate villi to terminal villi

immature intermediate villi predominate early (are involved in the growth of the villus tree) and mature to give rise to terminal villi (with a more extensive capillary network)

terminal villi comprise more than 50% of the villous surface and are the major sites of maternal-fetal exchange

stem villi serve as the support structure containing arteries and veins

36
Q

where do the two fetal umbilical arteries arise from?

A

from the two fetal iliac arteries

37
Q

what vessels supply fetal blood to the placenta?

A

two umbilical arteries

38
Q

describe the interaction between the fetal umbilical arteries and the placenta

A
  1. the two umbilical arteries contact the chorionic plate at the center and subsequently divide to send out about 20 branches radially over the placental surface
  2. each branch gives off a vertical branch to the stem villi
39
Q

describe the branching pattern of the umbilical vein

A

similar to umbilical arteries

each stem villus is supplied with a single artery and vein

40
Q

what types of vessels do intermediate villi contain?

A

contain arterioles and venules

41
Q

what types of vessels do terminal villi contain?

A

capillaries

42
Q

what arteries supply the maternal placenta?

A

uterine and ovarian arteries

these vessels anastomose and send 9-14 branches to the lateral margins of the uterus

within the myometrium, these vessels divide to form the arcuate arteries

43
Q

what are arcuate arteries?

A

vessels in the myometrium of the maternal placenta

pass circumferentially to the anterior and posterior uterine walls to meet with arcuate arteries on the opposite side

from the arcuate system rises the radial arteries

44
Q

describe the pathway of the radial arteries in the maternal placenta

A

pass deeper into the endometrium and give rise to the spiral and basal arteries

spiral arteries–supply intervillous space

basal arteries–supply the myometrium and decidua

45
Q

what type of blood surrounds the villi in the placenta?

A

well oxygenated maternal blood

this blood enters the intervillous space from spiral arteries in the decidua basalis

(the intervillous space is derived from the lacunae that developed int he syncytiotrophoblast in early placental development)

46
Q

how does maternal blood enter the intervillous space in the definitive placenta?

A

propelled into the intervillous space in jet-like streams travelling upward to the chorionic plate before percolating down through the villi towards the maternal venous drainage

47
Q

what three aspects are involved in placental maturation?

A
  1. increase in surface area for exchange
  2. closer approximation of maternal and fetal circulation
  3. increase and directed uterine blood flow

**the process of placental maturation works to optimize the opportunity for efficient maternal-fetal exchange, as fetal oxygen consumption is known to increase 10 fold over the duration of a pregnancy

48
Q

what types of transfer occur in the placenta?

A
  1. active transport
  2. facilitated diffusion
  3. passive diffusion
  4. pinocytosis
  5. osmosis
49
Q

what types of nutrients/materials are transported via the following mechanisms in the placenta?

  1. active transport
  2. facilitated diffusion
  3. passive diffusion
  4. pinocytosis
  5. osmosis
A
  1. amino acids, calcium, phosphorus, magnesium, ascorbic acid
  2. glucose, lactate
  3. oxygen, CO2, CO, water, insoluble fatty acids, ketone bodies, electrolytes
  4. LDL cholesterol, IgG, some fatty acids
  5. water
50
Q

what materials are excreted from the fetus to the placenta?

A

urea
uric acid
creatinine

excreted via diffusion

51
Q

what nutritional state does the mother enter during pregnancy in order to support the fetus?

A

a state of accelerated starvation

i. e–
1. decreased glucose and amino acids
2. increased fatty acids, ketone bodies and TAGs
3. increased insulin response to glucose
4. increased use of fat for energy

52
Q

what cells/structure carries out the endocrine functions of the placenta?

A

the syncytiotrophoblasts

53
Q

what protein hormones are produced by the placenta

A

HCG

HPL

54
Q

what is HCG? what is its structure and function? when is it detectable?

A

hormone produced by the placenta

structure similar to LH, with same alpha structure as LH, FSH, TSH

produced almost exclusively by syncytiotrophoblasts

detectable 8-9 days after ovulation–> serum levels double every 48 hours to 10 weeks; useful to determine risk factors or complications (i.e ectopic pregnancy, fetal demise, twin pregnancies)

functions to maintain the corpus luteum and therefore maintains progesterone secretion

at 6 weeks the placenta can take over progesterone production and therefore after 6 weeks HCG decreases

55
Q

what is HPL? what is its function?

A

protein hormone produced by the placenta

amount is proportional to placental mass–> rises steadily in the first 36 weeks

supports nutritional needs of the fetus by keeping nutrient supply constant to the fetus

  • -> maternal fasting state–incerases lipolysis resulting in increased FFAs and ketones
  • -> maternal fed state–anti-insulin action to increase circulating glucose and increase glucose to fetus

the clinical correlate is gestational diabetes

56
Q

what steroid hormones are produced by the placenta?

A
  1. progesterone
  2. estrogen
  3. corticosteroids
57
Q

what does placental progesterone production depend on?

A

depends on having maternal cholesterol as a precursor

58
Q

what is the role of progesterone produced by the placenta during pregnancy?

A

(initially progesterone is produced by the corpus luteum due to induction by HCG… after about 6 weeks the placenta takes over)

maintains uterine quiescence during pregnancy–> is is pro-gestation

  • decreases prostaglandin
  • smooth muscle relaxation
  • modulates the immune system

placental progesterone is a pool of corticosteroids for fetal adrenal synthesis

59
Q

what are the precursors for estrogen produced by the placenta in early pregnancy? in late pregnancy?

A

in early pregnancy it is maternal androgens

in alte pregnancy it is fetal androgens

60
Q

what is the role of estrogen produced by the placenta?

A

increased uterine blood flow and cardiac output –> peripheral vasodilation, regulate blood volume by stimulating RAAS

uterine preparedness for labour–> uterine contractions

prepare breasts for lactation

increased liver production of steroid hormone binding globulins

61
Q

what is the role of corticosteroids produced by the placenta?

A

fetal adrenal glands produce androgens using placental progesterone as the precursor

promote fetal lung maturation

promote maternal fluid expansion

62
Q

describe the formation of amniotic fluid and its transfer across the amnion in the first trimester

A
  • initial amniotic fluid is ISOTONIC with maternal plasma
  • it is a TRANSUDATE of both maternal plasma (from the uterine decidua via the amnion) and fetal plasma (through non-keratinized fetal skin or the umbilical cord)
  • fluid almost devoid of protein
  • by end of first trimester, there is about 50mL of fluid in the amniotic sac
63
Q

describe the formation of amniotic fluid and its transfer across the amnion in the second and third trimesters

A
  • beginning in second trimester, FETUS begins to contribute significantly to the amniotic fluid and the composition of it changes as a consequence
  • as the fetal kidneys mature, they begin to produce hypotonic urine which contains more urea, creatinine and uric acid than plasma
  • at term, the kidneys may produce up to 1L of urine per day
  • fetal RESPIRATORY tract actively secretes up to 250 mL of fluid per day at term
64
Q

describe the changes in amniotic fluid composition with increasing gestational age

A
  1. decreasing osmolality and sodium
  2. increasing urea, creatinine and uric acid
  3. increasing glycerophospholipids from lungs
  4. increasing particulate matter (desquamated fetal cells, lanugo, scalp hair, vernix caseosa)
  5. variation in protein content (protein increases until 24 weeks, stabilizes and the decreases after 32 weeks)
65
Q

what is the main source of amniotic fluid beginning in the second trimester?

A

fetal urine production

influenced by hormonal factors which explain why fluid volume changes based on fetal stress

66
Q

what are the two sources of fluid production during gestation?

A

fetal lung fluid production and fetal urine production

67
Q

describe the processing of fetal lung fluid

A

fetal breathing movements bring amniotic fluid in and out helping lung development and maturation

half of fluid produced in swallowed and the rest is excreted into amniotic fluid

68
Q

what are the two methods of fluid resorption during gestation?

A
  1. fetal swallowing–main route of fluid resorption, starts at 16 weeks; provides water and 10% of protein needs to fetus
  2. intramembranous flow–osmosis drags fluid into placental vasculature, final balancer of fluid production and resorption
69
Q

what three factors most affect maternal oxygen transport as it relates to pregnancy?

A
  1. uterine blood flow
  2. hemoglobin concentration and oxygen affiinity
  3. bohr effect
70
Q

describe changes to uterine blood flow during pregnancy, as medical conditions that can limit it

A
  • uterine blood flow increases around 10X throughout pregnancy, around 500-700 cc/min near term–> due to progressive vasodilution, and accounts for 20-25% of maternal cardiac output at term
  • medical conditions that can limit uterine blood flow: maternal hypotension, supine hypotensive syndrome, severe hemorrhage
71
Q

describe how hemoglobin concentration and oxygen affinity affect maternal oxygen transport

A
  • maternal arterial blood is almost always completely saturated with O2
  • maternal Hb has less O2 affinity than fetal Hb
  • maternal hypoxia (i.e due to pulmonary embolus or hypoventilation) can affect fetal oxygenation
72
Q

what is the bohr effect and how does it relate to maternal oxygen transport?

A
  • decreased pH, increased temperature and increased 2,3DPG all decrease Hb affinity to oxygen
  • in the intervillous space, fetal metabolites and CO2 pass from fetus to mother–> the intervillous space thus becomes more acidic, maternal curve shifts further to the right, facilitates O2 release to fetus (from mother)//fetal pH becomes less acidic, shifts fetal curve further left, facilitates O2 uptake
73
Q

describe the fetal circulatory pattern

A
  1. blood enters fetus through the umbilical veins–> umbilical arteries bring de-ox blood from fetus to placenta
  2. there are 3 fetal shunts:
    - ductus venosus bypasses the liver
    - foramen ovale delivers O2 rich blood from right side of heart to the left side for perfusion of brain
    - ductus arteriosus connects pulmonary artery to aorta (R ventricle therefore delivers less O2 blood relative to left ventricle to the rest of the body)
74
Q

why is the most O2 rich blood shunted thru the foramen ovale?

A

allows this blood to supply the brain directly

75
Q

list the essential components of placental oxygen transfer

A
  1. pO2 gradient and its determinants
  2. placental diffusion capacity for oxygen
  3. fetal hemoglobin dissociation
  4. uneven placental perfusion and shunting
76
Q

what is the mean pO2 of moms arterial blood?

A

100mmHg

77
Q

what is the mean pO2 of intervillous space?

A

50mmHg

78
Q

what is the mean pO2 of the fetus?

A

30mmHg

79
Q

how much of the oxygen that is delivered to the feto-placental unit at term is consumed by the placenta?

A

about 50% at term

80
Q

what are normal values for the following in pregnancy and labor?

  1. pH
  2. pCO2
  3. HCO3-
  4. BE
A
  1. 7.28 (7.2-7.38)
  2. 50 (40-50 mmHg)
  3. 22 (18-25 mEq/L)
  4. -3 (-5.5-0 mEq/L)
81
Q

on what does the fetus rely in order to clear acids and maintain pH?

A

placenta (as opposed to using lungs or kidneys)

82
Q

how would you tell if a fetus is acidotic, and whether the cause was respiratory or metabolic?

A

draw and analyze umbilical bord blood

83
Q

what two kinds of acids does the fetus produce?

A
  1. carbonic acid (H2CO3)

2. organic acids (lactic and ketoacids)

84
Q

describe the clearance of acids produced by the fetus

A
  1. fetal acids cross the placenta into the IVS where maternal blood lies–> decreases pH–> right bohr shift–> decreases Hb affinity for O2–> O2 travels from mother to fetus
  2. carbonic acid dissociates into CO2 + H2) and CO2 rapidly diffuses across the placenta
  3. organic acids result from anaerobic metabolism–> cross placenta more slowly than CO2 and the passage requires a pH dependent carrier–> this carrier is produced when fetal oxygenation is impaired (i.e in the cases of maternal hypotension, uterine hemorrhage, umbilical cord compression)
  4. maternal blood has higher affinity for CO2 since the mother creates a gradient via physiological hyperventilation
  5. if fetus is unable to exchange acids across the placenta in a sustained fashion, the fetus copes by using buffers (Hb and bicarb)–> this may eventually be overridden by acids causing deleterious effects on fetal wellbeing and newborn outcomes (i.e cerebral palsy)
85
Q

list normal changes to the cardiovascular system that occur in the mother during pregnancy

A
  1. cardiac output increases by 30-50%
  2. HR increases to about 80-90 bpm
  3. greater increase in HR during exercise than the rise in non-pregnant women
  4. cardiac output decreases rapidly after delivery, then more slowly and returns to pre-pregnancy levels about 6 weeks after delivery
  5. murmurs or palpitations may occur due to increased HR and cardiac output
  6. BP usually decreased in second trimester by may return to normal pre-pregnancy levels in the third
  7. enlarging uterus interferes with return of blood from legs and pelvic area to the heart–> may cause lower limb edema or varicose veins in legs or around vaginal area
86
Q

list normal changes to the hematologic system that occur in the mother during pregnancy

A
  1. blood volume increases by 50%
  2. uterus receives 20% of maternal blood supply
  3. amount of fluid in blood increases more than the number of RBCs, and therefore even though RBC # increases you may still notice mild anemia (which is normal)
  4. WBC # also increases slightly during pregnancy and increases ALOT during labor and the first few days post partum
87
Q

list normal changes to the respiratory system that occur in the mother during pregnancy

A
  1. high progesterone in pregnancy signals the brain to lower the level of CO2 in the blood –> results in tachypnea and hyperventilation to exhale more CO2–> may also breathe faster because uterus growth limits depth of breathing
  2. during exercise and exertion pregnant women may feel out of breath, especially towards the end of pregnancy
88
Q

list normal changes to the renal and urinary system that occur in the mother during pregnancy

A
  1. kidneys work harder throughout the pregnancy to filter the expanded blood volume–> max volume filtered by kidney achieved at 16-24 weeks and remains maximum until immediately before delivery
  2. kidney activity increases when a person lies down and decreases when a person stands up–this difference is amplified during pregnancy and is a reason that pregnant women need to urinate frequently when lying down
  3. if a pregnant woman lies on her left, less pressure is put by the uterus on the IVC and more blood can be returned from the pelvis and lower legs–> therefore increases the cardiac output and increases renal filtration of blood–> late in pregnancy lying on the left may also increase the need to urinate
  4. uterus also presses on the bladder reducing its size and causing it to thus fill more quickly–> results in increased urgency and frequency
89
Q

list normal changes to the GI system that occur in the mother during pregnancy

A
  1. nausea and vomiting (esp. in mornings)–> not sure why but may be due to high levels of estrogen and HCG; may be improved by changes in diet and eating habits/times/amounts
  2. heartburn, burping–> due to LES relaxation allowing the stomach contents to flow backward into the esophagus
  3. less acidic stomach during pregnancy
  4. enlarging uterus on the rectum and lower intestine may cause constipation –> progesterone also slows the peristaltic waves in the intestine; can be improved by high fiber diet with increased fluid intake, exercise
  5. hemorrhoids may result from pressure of enlarging uterus or from constipation
  6. may develop pica
90
Q

list normal changes to the skin that occur in the mother during pregnancy

A
  1. placenta produces melanin–> stimulates melanocytes–> results in the mask of pregnancy (melasma)–> blotchy, brown pigment that appears on forehead and cheeks; areola may also darken; linea alba can also darken
  2. stretch marks on abdomen
  3. spider angiomas on skin above waist
91
Q

list normal changes to the MSK system that occur in the mother during pregnancy

A
  1. joints and ligaments in the pelvis loosen and become more flexible to make room for enlarging uterus and prepare for delivery
  2. spine curves to balance the weight of the enlarging uterus
92
Q

list normal changes to the breasts that occur in the mother during pregnancy

A
  1. enlarge due to estrogen
  2. glands increase in number and gain ability to produce milk
  3. colostrum (thin, yellowish, milky discharge) is produced in the last weeks of pregnancy and the first few days post-partum–> this is rich in minerals and antibodies
93
Q

list normal changes to the female reproductive system that occur in the mother during pregnancy

A
  1. uterine enlargement–> above pelvis at 10 weeks, at navel at 20 weeks, lower edge of rib cage at 36 weeks
  2. vaginal discharge (normal being white or clear) increases–> if there is burning/itching/unusual color or smell is it NOT normal
  3. yeast infections are common during pregnancy
94
Q

list normal changes to the endocrine system that occur in the mother during pregnancy

A
  1. TSH –> increased amounts of T4 (increases HR, palpitations, perspiration, mood swings)
  2. estrogen and progesterone maintain pregnancy
  3. increased aldosterone and cortisol cause fluid retention
  4. HPL increases blood sugar (diabetes can appear or worsen during pregnancy)
95
Q

list the 3 positive tests for definitive diagnosis of pregnancy

A
  1. demonstration of fetal heart beat
  2. fetal movement
  3. visualization of fetus
96
Q

list the 5 probable indications of pregnancy

A
  1. enlarged uterus
  2. uterine and cervical changes
  3. palpation of fetus
  4. braxton hicks contractions
  5. positive beta hCG test
97
Q

list the 5 presumptive indications of pregnancy

A
  1. amenorrhea
  2. breast changes
  3. congestion of vagina
  4. skin changes
  5. common symptoms (nausea, fatigue, bladder irritability)
98
Q

what is the beta-hCG test?

A

pregnancy test

hCG is human chorionic gonadotropin –> glycoprotein made up of alpha and beta subunits

appears in maternal blood on day 8 or 9 post-conception and increases until 10 weeks

detected in urine (home pregnancy test) as early as 2-4 days before missed period (8 days post conception)

99
Q

what are the functions of hCG?

A

luteotropic to maintain corpus luteum

gonadotropic for fetal testicular development until 9-10 weeks

100
Q

how do you determine gestational age?

A
  1. dating–> menstrual age is embryonic age plus 2 weeks –> can determine due date using Naegele’s rule
  2. ultrasound–> measurement of fetal size compared to normal curves–> earlier scans are most accurate for dating (less than 14 weeks)
101
Q

what is naegele’s rule?

A

determines due date

LMP + 7 days - 3 months + 1 year

102
Q

in a non-obese patient, when can fetal cardiac activity be visualized?

A

5-6 weeks on transvaginal U/S

8 weeks on transabdominal U/S

103
Q

in a non-obese patient, when can fetal cardiac activity be heard?

A

10-12 weeks with trans-abdominal doptone auscultation

historically fetal stethoscopes were used

in later pregnancy may be able to hear with steth on maternal abdomen

104
Q

list risk factors for complications during pregnancy

A
  1. hypertension
  2. diabetes
  3. STIs
  4. pyelonephritis
  5. acute surgical problems (ie intra abdominal surgery occurring during pregnancy)
  6. genital tract abnormalities
  7. maternal age (too young or too old)
  8. maternal weight (underweight or obese)
  9. maternal height (less than 152 cm because of small pelvis)
  10. exposure to teratogens
  11. prior stillbirth
  12. prior preterm delivery
  13. prior neonate with a genetic or congenital disorder
  14. polyhydramnios and oligohydramnios
  15. mutifetal pregnancy
  16. prior birth injury
105
Q

look at the BCPHP maternity care guidelines

A

www.bcprenatalscreening.ca/sites/prenatal2/files/guidelines_19.pdf

106
Q

what do you do at the first prenatal visit?

A
  1. confirm pregnancy–> do not need repeat hCG test if one was done at home unless there is some uncertainty with the patient testing–> can confirm with hx and physical and ultimately a routine U/S
  2. medical hx
  3. risk assessment
  4. physical exam–> general physical, signs of pregnancy, pelvic exam (uterine size, pap smear and swabs)
107
Q

what are the recommendations that should be made in terms of lifestyle etc… for pregnant women?

A
  1. smoking cessation
  2. counsel about the effects of alcohol and illicit drugs
  3. physical activity
  4. sexuality
  5. supplements (folic acid and iron)
  6. work environment
108
Q

what are routine investigations for prenatal care?

A
weight
BP
urine dip for protein
SFH
fetal HR
109
Q

how is fetal growth monitored routinely?

A

SFH +/- ultrasound

SFH is symphyseal-fundal height

  • normal values–> 12 weeks at pubic symphysis, 16 weeks midway between pubic symphysis and umbilicus, 20 weeks at umbilicus
  • if small SFH and lack of growth, ask about fetal movement as an indirect measure of fetal oxygenation and wellbeing
  • *U/S is indicated if more than or equal to 3 cm below or above normal SFH
  • U/S not indicated for a single elevated BP but is indicated for confirmed persistent HTN
110
Q

what are the routine screening tests done in the third trimester?

A

gestational diabetes

group B strep–> 35-37 weeks vaginal-rectal swab (antibiotics in labor… pen G)

111
Q

what is assessed on U/S during pregnancy?

A
  1. fetal measurements (head circumference, abdominal circumference, femur length) and compare it to norms
  2. amniotic fluid volume
  3. assess fetal wellbeing by observing fetal movement, tone, breathing (all require fetus to be well-oxygenated and perfused)
112
Q

is there a definitive theory as to why the onset of labour occurs?

A

while there are many theories as to why the onset of labour occurs, very little is known–> the sheep model has been used extensively in the past, but unlike humans, there is more known in that model about the onset of labour

113
Q

describe the events that lead to the spontaneous onset of labour

A
  1. progesterone levels do not fall (not do estradiol levels)–administration of progesterone does NOT prevent preterm labour and giving estrogen does NOT induce labour in pregnant women
  2. systemic levels of prostaglandin metabolites, local levels of arachadonic acid, calcium dependent phospholipases or relaxin do not rise until active labour itself is in progress
  3. cortisol levels remain unchanged
  4. oxytocin only rises once labour has begun
114
Q

what is the role of uterotropins in labour? give examples of 3 uterotropins.

A

they set the stage for uterine contractions and cervical changes

estrogen
relaxin
arachadonic acid

115
Q

what is the role of uterotonins in labour? give examples of 3 uterotonins.

A

agents that are directly involved in causing myometrial smooth muscle cells to contract by increasing intracellular calcium concentration

oxytocin
prostaglandins
endothelin-1

116
Q

describe the role of oxytocin in labour and where it is released from

A

produced in hypothalamus–> released by the posterior pituitary–> levels only rise once labour has BEGUN

causes peristaltic contractions of uterine smooth muscle by increasing intracellular calcium

stimulates PGF2

receptors that exist on myometrial cell membranes increase near term–> are increased by estrogen and decreased by progesterone

cause increased gap junctions between myometrial cells

increases coordination of contractions

clinical correlate: braxton hicks contractions are disorganized contractions in T2 or early T3–> gap junctions are not yet organized by oxytocin so do not have coordinated contractions leading to labour

117
Q

describe the role of prostaglandins in labour. what are the two types we care about? where are they released from? where do they each act?

A

released from the decidua, amnion or chorion

arachidonic acid–> PGE2 and PGF2 (stimulated by estradiol)

PGE2–> acts at cervix–> rearrange collagen to provide less resistance for downward expulsion (this is inhibited by progesterone until levels drop at onset of labour)

PGF2–> more active in contraction, released when lower uterine segment thins–> inflammatory reaction in response to pressure/trauma (i.e sex, fetal head on cervix, manual stimulation of cervix) –> increased intracellular calcium due to PGF2 leads to increased contractions

sensitive myometrial cells to oxytocin–> resulting in myometrial contraction

118
Q

what is the role of relaxin in labour? where is it released from?

A

released from ovary

involved in cervial ripening with PGE2

119
Q

what is the role of endothelin-1 in labour?

A

present in myometrium, important for the involution of uterus after placental delivery

120
Q

what is the role of estrogens in labour?

A

increase myometrial contractility and stimulate the release of oxytocin and PGs

121
Q

uterotropin or uterotonin?

estrogen

A

uterotropin

122
Q

uterotropin or uterotonin?

oxytocin

A

uterotonin

123
Q

uterotropin or uterotonin?

endothelin-1

A

uterotonin

124
Q

uterotropin or uterotonin?

relaxin

A

uterotropin

125
Q

uterotropin or uterotonin?

calcium dependent phospholipases

A

uterotropin

126
Q

uterotropin or uterotonin?

prostaglandins

A

uterotonin

127
Q

uterotropin or uterotonin?

arachidonic acids conversion to prostaglandins

A

uterotropin

128
Q

how many phases are there in labour?

A

3

129
Q

what happens in phase 0 of labour?

A

uterine quiescence

contractile tranquility

130
Q

what happens in phase 1 of labour?

A

uterine preparedness and functional change in myometrium and cervix

in sheep: fetal CRH–> ACTH–> cortisol–> placental estrogen–> dampens progesterone, decreasing progesterone’s role in uterine quiescence–> increased PG produced in amnion and chorion–> increased gap junction formation in myometrial cells–> coordinated, regular uterine contractions

in humans, the main changes are: increase in myometrial cells contractile responsiveness, breakdown of collagen fibers in the cervix to thin and dilate in reponse to regular contractions originating in the uterine fundus

131
Q

what happens in phase 2 of labour? list a brief description of what happens in each of the 4 stages of phase 2

A

ACTIVE LABOR, progessive cervical dilatation, and fetal delivery

  • uterus becomes thicker in upper part and thinner in lower part to assist downward fetal movement
  • contractions caused by anything that increases intracellular calcium in smooth muscles
  • relaxation is caused by agents increasing intracellular cAMP levels

stage 1–> onset of involuntary painful contractions until full dilation of the cervix

stage 2–> full dilation to expulsion of the fetus (uterine contractions + pushing by the mother directs the fetus down and out)

stage 3–> delivery of fetus to delivery of placenta

stage 4–> delivery of placenta to stabilization of mother

132
Q

describe stage 1 of phase 2 (active) of labour

A

onset of involuntary painful contractions until full dilation of the cervix

latent phase–> onset of contractions every 5 minutes until the cervix is dilated to 4 cm

active phase–> 4 cm dilation with contractions every few minutes

133
Q

describe stage 2 of phase 2 (active) of labour

A

full dilation to expulsion of the fetus (uterine contractions + pushing by the mother directs the fetus down and out)

can last anywhere from 20 min to 3 hours

the cardinal movements of labour occur

134
Q

what are the cardinal movements of labour?

A

occur in stage 2 of phase 2 of labour
(look at diagram on page 54 of repro review notes)

  1. before engagement
  2. engagement, flexion, descent
  3. descent, rotation
  4. complete rotation, early extension
  5. complete extension
  6. restitution
  7. anterior shoulder delivery
  8. posterior shoulder delivery
135
Q

describe stage 3 of phase 2 (active) of labour

A

delivery of fetus to delivery of placenta

uterus continues to contract after fetal delivery, compresses placenta

separates at decidua spongiosa

blood clot forms, furthering separation

placenta slides into lower uterus

pushing/gentle traction expels the placenta

lasts usually 15-30 min, indicated by rush of blood, umbilical cord lengthening, fundus rises up

136
Q

describe stage 4 of phase 2 (active) of labour

A

delivery of placenta to stabilization of mother

137
Q

what happens in phase 3 of labour?

A

uterine involution; “fertility” restored

  • 6 weeks following delivery when physiological changes revert to non-pregnant state
  • uterus involution–> intermittent oxytocin causes contractions–> “after pains”–> uterus shrinks in size–> 4 weeks post delivery uterus returns to non-pregnant weight (100g)
  • cervix–> cervix slowly lengthens and endocervical canal never completely closes
  • this phase is complete once menses resume (dependent on breastfeeding)
138
Q

what is the lochia?

A

decidua basalis–> basal layer of endometrium, superficial layer grows on top–> sloughed (normal vaginal discharge post partum is called the lochia)

will be red then yellow then white

139
Q

list the normal maternal physiological changes of the postpartum period in the:
uterus

A

involution of the uterus

  • the uterus at delivery is about 1 kg, and by 3 weeks post delivery its 300 g
  • this change occurs due to oxytocin release, causing continued contractions that lead to a decrease in the myometrial cell size
  • the cervix retracts to its normal position but the endocervical canal never completely closes again (internal os closes, external os remains slightly open)
  • there are uterine discharges within the first few days post-delivery–> lochia rubra for first few days (red), lochia serosa after 3-4 days (paler) and lochia alba by the 10th day (white or yellow white)
140
Q

list the normal maternal physiological changes of the postpartum period in the:
breasts/lactation system

A
  • after the placenta falls/is tugged out, estrogen and progesterone drop–> increased prolactin release
  • increased prolactin increases alpha-lactalbumin, which stimulates lactose synthesis
  • lactose is the major carbohydrate in breast milk, which includes casein, lactalbumin and beta-lactoglobulin as well as IgA for passive immunity
  • the baby’s suckling stimulates oxytocin release –> myoepithelial cell contraction–> milk ejection
141
Q

list the normal maternal physiological changes of the postpartum period in the:
vagina

A

supportive tissues of the pelvic floor regain their tone (but are never as “toned” as they once were”

142
Q

list the normal maternal physiological changes of the postpartum period in the:
cardiovascular system

A
  • after delivery, there’s an increase in the peripheral resistance, due to removal of the low pressure utero-placental shunt
  • the cardiac output rises in the first two days, but then returns to normal during the next two weeks–> there is increased diuresis to eliminate the increased blood volume and the ECF leading to 6-7 kg weight loss on top of the 6-7 kgs lost from the baby and bits (placenta, blood)
  • the blood vessels in the pelvis that supplied the uterus and pelvis during pregnancy decrease in size
  • the coagulation factors decrease over 6 weeks, and a granulocytic leukocytosis may be seen in the immediate post partum period
143
Q

list the normal maternal physiological changes of the postpartum period in the:
other systems/miscellaneous

A
  • post partum blues (possible due to hormonal changes)–common but usually resolve without consequence
  • abdominal wall muscles relax
  • overstretched elastic fibers remain as striae
  • weight gain of more than 15 kgs during pregnancy becomes post partum weight gain
  • in the absence of breast feeding, menses resume in 6-8 weeks–> high prolactin with breast feeding inhibits estrogen release and menses may not recur for months
144
Q

what is the global incidence of unintended pregnancy?

A

80 million women per year worldwide have unintended pregnancies, of which, 45 million are terminated

145
Q

what is the incidence of unintended pregnancy in the USA?

A

about 3 million women per year (49%) of which 600 000 (20%) are terminated via abortion and 200 000 (7%) are terminated due to fetal loss

an estimated 1/3 of women will have an abortion by age 45

146
Q

what is the incidence of unintended pregnancy in Canada?

A

31% of women entering menopause in 2005 have had an abortion

rate of apportion is 14.1 per 1000 women aged 15-44

abortion ratio is 28.3 per 100 live births

147
Q

unintended pregnancies are the result of what?

A

failed or unavailable contraception

148
Q

what are the surgical and medical abortion techniques available for “early” (first trimester) abortion?

A

surgical: suction aspiration (it is certain and can be done in a single visit)
medical: medication abortion (it is private and isn’t surgery)

149
Q

what are the surgical and medical abortion techniques available for abortion beyond the first trimester?

A

surgical: dilation and evacuation (lower risk, and its quick… no labour)
medical: induction abortion (intact, no surgery)

150
Q

describe the safety of abortions

A
  • legally induced abortion is safer than carrying a pregnancy to term
  • future fertility after an induced abortion is similar to that after a miscarriage at the same gestation
  • no association with breast cancer
  • first trimester abortions pose no risk to fertility, ectopic pregnancy, miscarriage, birth defect, preterm or low birth weight delivery
151
Q

what are some of the reproductive options available to women in canada?

A
  1. abortion clinics
  2. contraception and sexual health clinics
  3. toll free counseling and referral
  4. online resources
152
Q

what is the physician’s role in pregnancy counseling?

A
  • no discrimination should be directed against doctors who do not perform or assist at induced abortions
  • no discrimination should be directed against doctors who provide abortion services
  • patients should be provided with the option of full and immediate counselling services in the event of unwanted pregnancy –> there should be NO DELAY in the provision of services
  • inform your patient when your personal values would influence the recommendations or practice of any medical procedure that the patient needs or wants
  • do not discriminate against any patient
  • parental consent is NOT required for abortion services in a minor–the patients need only to be deemed competent
153
Q

why do we care about the placenta?

A

placental implantation, maturation and pathophysiology have significant implications on the developing fetus, newborn and mom

improperly developed placenta can result in….

  • spontaneous abortion and miscarriage
  • fetal growth issues
  • nutrition and oxygenation problems
  • prematurity
  • maternal risks (antepartum hemorrhage, postpartum hemorrhage, pre-eclampsia)
154
Q

what are some of the things that can go wrong with the placenta? (lecture slides)

A
  1. shallow/inadequate implantation –> miscarriage, IVF failure, fetal growth restriction, preeclampsia
  2. abnormal location–> ectopic, previa
  3. uncontrolled invasion–> accreta
155
Q

what two synchronous processes are required for proper placental implantation?

A
  1. uterine preparation (decidual reaction)

2. embryo development and ability to interact with the endometrium

156
Q

what % of all conceptions fail at the critical time of implantation?

A

50%

may have abnormal karyotype

IVF has higher failure rate likely due to issues with implantation

157
Q

what two parts of the decidua combine as the embryo grows to form the decidua vera?

A

decidua parietalis and the decidua capsularis

158
Q

what part of the decidua is the implantation site?

A

decidua basalis

eventually becomes the maternal portion of the developing placenta

159
Q

what is placenta previa?

A

when the placenta implants over the cervix

160
Q

what do you call it when the placenta implants in a site other than the fundus (normal) or over the cervix (previa)?

A

ectopic

161
Q

describe the parts of the day 5 zygote/blastocyst

A

inner cell mass–> compacts to one side to form the embryonic pole

fluid filled cavity–> blastocoele

outer cell mass–> trophoblast

162
Q

what two cell types are trophoblasts destined to become?

A
  1. cytotrophoblasts (progenitor cells)

2. syncytiotrophoblasts

163
Q

what are cytotrophoblasts?

A

derived from trophoblasts/outer cell mass of blastocyst

they are progenitor cells

there are villus cytotrophoblasts and extravillus cytotrophoblasts

164
Q

what are syncytiotrophoblasts?

A
  • giant, multinuclear cells formed by fusion of cytotrophoblasts
  • terminally differentiated
  • invasion of endometrium
165
Q

how do you investigate cytotrophoblast invasion clinically?

A

via uterine artery dopplers

166
Q

what is the accreta spectrum?

A

pathologic deep invasion of cytotrophoblasts

167
Q

what are some risk factors for pathologic deep invasion of cytotrophoblasts?

A
  1. prior C-section or uterine surgery (uterine scar becomes a site of uncontrolled invasion)
  2. placenta previa (lower uterine segment implantation more likely to have deep invasion)
168
Q

when is accreta often diagnosed? why is this relevant?

A

often not diagnosed until delivery when you are unable to deliver the placenta and this leads to postpartum hemorrhage, hysterectomy and even death

maternal death with accreta reported up to 7%

169
Q

what factors influence fetal oxygenation?

A
  1. maternal oxygen capacity
  2. uterine blood flow
  3. placental oxygen transfer
  4. umbilical cord blood flow
  5. fetal oxygen capacity and fetal circulation
170
Q

what determines maternal oxygenation?

A

this is the total oxygen content in arterial blood

  1. hemoglobin concentration and saturation–> maternal arterial blood is almost always completely saturated with oxygen
  2. hemoglobin’s oxygen affinity –> this is itself impacted by temperature, acidity, and 2,3-DPG levels within RBCs
  3. oxygen dissolved in plasma
171
Q

what is the volume of uterine blood flow near term?

A

500-700 cc/min

due to progressive vasodilation

172
Q

is uterine blood flow autoregulated?

A

no–> depends on maternal BP

173
Q

what two factors determine placental perfusion?

A
  1. uterine blood flow

2. placental resistance

174
Q

what are 3 reasons not all the oxygen from the intervillous space gets to the fetus?

A
  1. shunting (oxygen is diverted to the placenta and the uterus itself for consumption–10-30% used by the placenta itself)
  2. uneven placental perfusion
  3. diffusing capacity of the placenta for oxygen
175
Q

what drives oxygen transfer from mother to fetus?

A
  1. oxygen gradient between mom and fetus
  2. fetal Hb has higher O2 affinity than maternal Hb
  3. Bohr effect
176
Q

why is the fetal O2-Hb dissociation curve placed to the left of the maternal curve?

A

because of fetal Hb’s higher affinity for oxygen

177
Q

what vessel carries blood from the placenta to the fetus?

A

1 umbilical vein

178
Q

what vessel carries blood from the fetus to the placenta?

A

2 umbilical arteries

179
Q

how much oxygen can fetal blood carry to tissues compared to the mother? why is this the case?

A

despite the low pO2, fetal blood is able to transport roughly the same quantity of oxygen to tissues as mother because the fetus has

  1. higher Hb concentration than adult
  2. Hb with higher O2-carrying capacity than adult
  3. higher cardiac output, so greater perfusion of organs
180
Q

who has more hemoglobin, fetus or mom?

A

fetus

fetus also has more RBCs and more capillaries per unit of tissue

181
Q

how does fetal hemoglobin differ from adult?

A

different globin chains–> gamma instead of beta (HbF)

erythrocytes that contain HbF bind more O2 than those with HbA (therefore fetus has higher oxygen affinity than adult

182
Q

how does fetal hemoglobin differ from adult?

A

different globin chains–> gamma instead of beta (HbF)

erythrocytes that contain HbF bind more O2 than those with HbA (therefore fetus has higher oxygen affinity than adult

183
Q

how does the function of the fetal heart chambers compare to adults?

A

in the fetus the chambers work in parallel and not in series as in an adult

i.e the left ventricle supplies highly oxygenated blood to the brain and heart whereas the right ventricle supplies less oxygenated blood to the rest of the body

184
Q

describe the pathway of fetal circulation including the shunts and their purpose

A
  1. highly O2 blood comes from the placenta to the fetus via the umbilical vein
  2. this blood is directed to the IVC via a shunt–> DUCTUS VENOSUS (allows blood to travel directly to heart and thus straight to brain)
  3. cardiac ventricles work in parallel–> separate circulations maintained by shunt between the atria–> FORAMEN OVALE (allows highly O2 blood to move from right atrium to left atrium to left ventricle to supply brain and heart)
  4. 90% of blood from right ventricle bypasses the lungs thru the DUCTUS ARTERIOSUS which passes blood from the pulmonary artery to the aorta (blood goes to body and back to placenta)
185
Q

how does the fetus form carbonic acid?

A

produced during normal, oxidative metabolism

186
Q

how does the fetus form lactic acid (and other organic acids)?

A

results from anaeobic metabolism and so is produced when fetal oxygenation is impaired

organic acids cross the placenta more slowly than CO2 (hours versus seconds)

187
Q

what would you see in the fetus if blood flow is interrupted for a short period of time?

A

i.e placental abruption, cord compression

fetal pH drops
CO2 rises
metabolism acid base status remains UNCHANGED (“respiratory acidosis”)

188
Q

what do you see in the fetus if oxygen lack is sustained?

A

fetus decreases its O2 consumption
redistributes blood flow to “vital organs”
relies partly on anaerobic metabolism to meet energy needs and you get lactic acid

189
Q

how does the fetus deal with excess organic acids?

A

buffers them with Hb and bicarb

if too much lactic acid is produced, this can overwhelm the buffer system and the system gets depleted leading to metabolic acidosis

190
Q

what value corresponds to pathologic fetal acidemia?

A

pH less than 7

increased risk of brain injury, seizures, need for CPR, NICU admin

191
Q

what values do you look at to differentiate between respiratory and metabolic acidosis in the newborn?

A

pCO2 to see if element of respiratory acidosis

HCO3- and BE to see if element of metabolic acidosis

192
Q

what values would you associate with newborn metabolic acidosis?

A

pH–low (less than 7.2)
pCO2–normal (40-50mmHg)
HCO3—low (less than 18)
BE–large (-6 or larger) **-12 or larger is significant

193
Q

what values would you associate with newborn mixed acidosis?

A

more commonly seen than pure metabolic acidosis

pH–low
pCO2–high (more than 60)
HCO3–low (less than 18)
BE–large (-6 or larger)

194
Q

which uses more energy, the placenta or the fetus?

A

placenta

1/2 of oxygen and 2/3 of glucose delivered to the uterus is used by the placenta for

  1. energy storage
  2. production
  3. transport
195
Q

what does the placenta use energy to do?

A
  1. energy storage–placenta synthesizes glycogen, which is stores as an energy reserve
  2. production–of proteins and steroids
  3. transport–active transport of some elements requires energy
196
Q

what types of substances commonly transfer thru the placenta via simple diffusion?

A
  1. large gradient between maternal and fetal blood
  2. low molecular weight
  3. minimal electric charge
  4. high lipid solubility
197
Q

why cant blood flow within the placenta be autoregulated?

A

because maternal blood is in the intervillous space and not within vessels (cannot vasoconstrict or vasodilate to alter blood flow)

198
Q

when does the placenta start making glucose?

A

not until late gestation

199
Q

is glucose transfer by the placenta insulin dependent?

A

no…. facilitate diffusion with glucose receptors on the placenta; non-energy dependent and non-insulin depenent

this process is more efficient than simple diffusion alone at ensuring adequate glucose to fetus

**pregnancy itself is a relative state of insulin resistance which increases the glucose available to the fetus

200
Q

why dont you use ACEi during pregnancy?

A

teratogenic

201
Q

what does HPL stand for? (the hormone)

A

human placental lactogen

202
Q

what is the function of amniotic fluid?

A
  1. cushions fetus from trauma
  2. prevents compression of the umbilical cord
  3. allows room for the fetus to grow and move
  4. important for limb development
  5. important for fetal LUNG development
  6. bacteriostatic properties prevent intra-amniotic infection
  7. temperature homeostasis
203
Q

why do fetal lungs produce fluid?

A

to expand the developing lungs to facilitate their growth

200mL/day

excess fluid leaves the lungs during breathing movements

204
Q

what is a common medicine that can cause oligohydramnios (too little amniotic fluid)?

A

maternal NSAID use

205
Q

what malformations/conditions can be caused due to too little amniotic fluid?

A
  1. limb contractures
  2. facial deformities
  3. pulmonary hypoplasia
  4. umbilical cord compression
  5. prematurity (iatrogenic)
  6. death
206
Q

can oligohydramnios be treated?

A

not generally