M2-Lecture1 Flashcards

1
Q

Preconception period is:

A

Period preceeding, including and immediately following human conception.

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2
Q

Prenatal period

A

Fertilization has occured and zygote is formed

Period between conception & birth

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3
Q

Perinatal period

A

Period immediately before and after birth.

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4
Q

Which trimester includes important developmental milestones and give examples:

A

First

Fertilization, pre-embryonic & embryonic period.

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5
Q

In first trimester basic structure of organs and tissues forms, what is this called?

A

Organogenesis

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6
Q

First trimester name of the developing baby:

Second trimester and third trimester: Fetal

A

Embryonic

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7
Q

What are finger-like projections that help guide the egg from the ovary into the fallopian tube after ovulation facilitating the meeting of egg & sperm for fertilization:

A

Fimbria

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8
Q

On what day after fertilization does the morula become blastocyst (dividing cells with central cavity filled with fluid - blastocoel:

A

Fifth day

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9
Q

What is a solid ball of cells that forms after the fertilization of an egg and the first few rounds of cell division, and is surrounded by ZP (16 cells)?

A

Morula

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10
Q

What does the blastocyst form into:

A
  • Trophectoderm (outer layer): Placenta (trophoblast cells) & fetal membranes.
  • Inner mass at one pole that will form the embryo

Fluid filled cavity (overall structure and deve. of embryo)

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10
Q

What is the outerlayer of the blastocyst?

A

Trophectoderm

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11
Q

What do uterine secretions provide to the blastocyst following the multiplying of the inner & outer cell masses:

A

Oxygen & metabolic substrates

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12
Q

Because the uterine secretions are inadequate, that’s why within 24 hours of hatching or day 6 after fertilization, the blastocyst implants in uterine lining, which has access to glycogen filled stromal cells (which supply nutrients). T/F

A

True

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13
Q

Gylcogen filled stromal cells are necessary for continued growth. T/F

A

True

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14
Q

Sperm can remain in the uterus for several days?

A

Yes

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15
Q

Sperm penetration causes zona pellucida to become impermeable by other sperm. what is this called?

A

Cortical reaction

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16
Q

How does sperm penetrate the ZP:

A

Acrosome of sperm binds to ZP, specifically ZP3 protein. Enzymes hyaluronidase and acrosin are released.

These enzymes help the sperm penetrate the ZP.

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17
Q

What fast block of the ploysperms?

A

Depolarization of egg’s membrane

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18
Q

The slow block involves:

A

Cortical reaction, where cortical granules release substances that modify ZP

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19
Q

Zygote fusion of two gametes, 46 chromosomes, divides by:

A

Mitosis

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20
Q

When does implantation occur:

A

By the end of first week. Blastocyst implants in uterine lining.

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21
Q

When the inner mass cell forms two-layered disc of embryonic cells, what is the fluid filled component btw. it & the trophoblast?

A

Amniotic cavity

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22
Q

Briefly explain what occurs during embryonic week 2 (GA week 4) development - early stages of embryonic deve.:

A
  • Inner cell mass forms two-layered disc of embryonic cells (Bilaminar embryonic disc)

Upper Layer: Epiblast

  • Develops into amnion, which fill with amniotic fluid
  • Also forms the embryo.

Lower Layer: hypoblast

  • Forms the yolk sac
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23
Q

What does the amniotic fluid contain?

A

Initially maternal plasma & later fetal urine.

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24
Q

Function of the amniotic fluid:

A

Protects embryo and allows movement.

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25
Q

During week 3, the yolk sac - allantois, contributing to the umbilical cord structure & the Chorion, outermost membrane surrounds all and plays key role in placenta development. T/F

A

True

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25
Q

The function of the yolk sac:

A

Provides early nutrition & blood circulation until placenta takes over in week 4.

Source of blood & germ cells.

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26
Q

Name the two layers that form when the trophoblast divides:

A

syncytiotrophoblast and cytotrophoblast

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27
Q

What consists of individual mononucleated cells that arise from the trophoblast after implantation.

A

Cytotrophoblast

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28
Q

What is formed by the fusion of cytotrophoblast cells, creating a multinucleated layer that invades the uterine wall. and nutrient and gas exchange btw. mother & embryo, produces hormones like hCG.

A

Syncytiotrophoblast

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29
Q

How can pregnancy be clinically detected:

A

hCG - corpus luteum (helps sustain the corpus luteum (produces progesterone and estrogen) from degradation.

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30
Q

When does embryonic disc (epiblast) differentiate into germ layers:

A

During embryonic week 3 (GA Week 5)

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31
Q

Name the three germ layers (kown as trilaminar embryonic disc):

A

Ectoderm

Mesoderm

Endoderm

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32
Q

When does the fetal begin to assume human shape:

A

56 days (8 weeks)

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33
Q

During the 56 days/8 weeks, a lot of rogans are formed but not fully differentiated. T/F

A

True

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34
Q

The first 8 weeks of embryonic period are very critical because of risk of deformities, miscarriage, and neural tube defects. T/F and what’s needed.

A

True

Folic acid

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35
Q

Embryological events during first 8 weeks:

A

Organs form from the three germ tissues. basic body plan.

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36
Q

Where is folic acid most abundant:

A

In Dark leafy green vegetables and spinach

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37
Q

Btw. which weeks does a women first learn of pregnancy?

A

Weeks 3-8

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38
Q

Thalidomide is given to cancer patients and why?

A

It prevents formation of blood vessel, so that tumors do not use the nutrients to spread.

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39
Q

External genital develop late? T/F

A

True

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40
Q

Each germ layer gives rise to specific tissue types & organs. T/F

A

True

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41
Q

What is the formation of organs from germ layers following gastrulation:

A

Organogenesis

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42
Q

Organogenesis occurs mainly during embryonic week 4-8 (GA 6-10).

A
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43
Q

During embryonic weeks 4-8, the embryo is most sensitive to harmful factors, such as (ex. alcohol, radiation, infectious agents, drugs, nutritional supplements, etc.) T/F

A

True

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44
Q

Totipotent (egg) gives rise to germ layers (pluripotent) then different organs (multipotent). T/F

A

True

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45
Q

What do endoderm (inner layer) give rise to:

A

lung cells
Thyroid
digestive cells

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46
Q

What do mesoderm (middle layer) give rise to:

A

Cardiac muscle

Skeletal muscle

Tubule cells

RBC

Smooth muscle

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47
Q

Endoderm, ectoderm and mesoderm give rise to specialized cells by epigenetics? T/F

A

True

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47
Q

Ectoderm (outer layer) give rise to:

A

Skin cells

Neurons (nerve cells)

Pigment cells

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47
Q

Describe the steps of placenta formation (placentation):

A

Implantation days 5-6:
blastocyst implants into uterine wall

Trophoblast differentiation: ○ Cytotrophoblast:
Syncytiotrophoblast:

Formation of chorion (week 2-3): trophoblast & mesoderm combine to form it.

Vascularization: blood vessels begin to form within the chorion

Mature placenta (weeks 4 and beyond).

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48
Q

Around week 12, the placenta becomes fully functional. T/F

A

True

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49
Q

Placenta is the vital organ of pregnancy. T/F

A

True

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50
Q

Placenta is responsible for all maternal-fetal exchange? T/F

A

True

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51
Q

What organs have later development:

A

Neural
Genital
Respiratory
Bones

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51
Q

What is the placenta involved in:

A

Metabolism
Barrier
Endocrine
Immune

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52
Q

What occurs in the second & third trimesters:

A

Includes fetal period
Growth & differentiation of formed organs
Growth in fetal size and length (2nd trimester)
Growth in fetal weight (3rd trimester)

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53
Q

What happens during growth in fetal weight:

A

Deposition of subcutaneous fat

54
Q

Characteristic of buckle fracture:

A

bulging or “buckle” of of the bone rather than complete break

54
Q

What is the most common fracture seen in children (but less common in fetuses due to flexibility of developing bones):

A

Buckle fracture

55
Q

What is the process of giving birth to an offspring called:

A

Parturition

56
Q

Describe the steps of parturition:

A
  • Sequential, changes in myometrium, decidua & cervix
  • Days to weeks
  • Release from the inhibitory effects of pregnancy on the myometrium (lower progestrone)
57
Q

Indicators of labor based on clinical diagnosis:

A

Uterine contraction increasing in frequency & intensity

Cervical effacement & dilation

57
Q

Parturition is initiated by the fetus: T/F

A

True

58
Q

Phases 1 of parturition:

A

Phase 1: quiescent phase (by progestrone & PGI2, relaxin, PtHrP, calcitonin gene-related peptide, vasoactive intestinal peptide and nitric oxide (NO).

59
Q

What’s the role of the components of phase 1:

A

To inhibit release of intracellular calcium for myometrial contractility.

60
Q

Phase 2 of parturition:

A

Activation of uterine function

Rise in estrogen & CRH

61
Q

The impact of rise in estrogen & CRH:

A

May lead to up-regulation of genes required for contraction during mechanical stretch.These CAPs include connexin 43, prostaglandin and oxytocin receptors (OTRs).

62
Q

Phase 3 of parturition:

A

Stimulation of uterus by uterotonics including prostaglandins, oxytocin, & CRH, cytokines.

63
Q

During parturition there is increased synthesis of cytokines resembling inflammation: T/F

A

True

64
Q

Phase 4 of parturition:

A

Involution phase - after the delivery of the fetus & placenta.

Effects of oxytocin

65
Q

Parturiton mechanisms:

A

Progesterone withdrawal

Estrogen bioavailability

Responsiveness of myometrium to prostaglandins & oxytocin

CRH & HPA axin activation

Uterine stretch

66
Q

During parturition, progesterone may still be high, but receptors are removed. T/F

A

True

67
Q

What is the primary hormone of pregnancy:

A

Progesterone

68
Q

Progesterone is made by both placenta (takes over) & corpus luteum during pregnancy. T/F

A

True

69
Q

Progesterone sustains uterine quiescence throughout pregnancy. T/F

A

True

70
Q

During pregnancy there is hyperesterogenic state. T/F

A

True

71
Q

The placenta is the primary source of estrogen once stimulated by maternal & fetal adrenal glands: T/F

A

True

71
Q

Concentrations of estrogen increase with gestational age:

A

True

72
Q

Estrogen promote myometrial changes or uterine contraction. T/F

A

True

73
Q

Mechanisms of myometrial changes:

A

Increase of prostaglandin receptors

high Oxytocin receptors

high myometrial gap junctions

up-regulate enzymes responsible for muscle contractions

74
Q

Estrogen promotes cervical rippening?

A

Yes

75
Q

During parturition, on what receptors does CRH act upon?

A

Hormonal, vascular, & inflammatory

75
Q

What is the most common neuropeptides involved in parturition?

A

CRH

76
Q

Placenta is capable of synthesizing & releasing many neurohormones, & neuropeptides. T/F

A

True

76
Q

What share sequences homologies with CRH & have similar biological effects:

A

Urocortins (Ucn, Ucn2, Ucn3)

77
Q

Role/function of neurohormones and neuropeptides:

A

Act locally in modulating pituitary-like hormones, & resemble the HP target gland axes

78
Q

Women who plan to get pregnant receive blood test. Why?

A

To make sure that they don’t have hypothyroidism.

79
Q

Thalidomide was only teratogenic in humans. T/F

A

True

80
Q

Fetal blood does not touch maternal blood (tree-like structure). T/F

A

True

81
Q

The syncytiotrophoblast is the layer that forms the villi. the syncytiotrophoblast extends out into the uterine tissue, creating the finger-like projections known as chorionic villi. These villi are essential for increasing the surface area for maternal-fetal exchange of nutrients, gases, and waste products. The underlying cytotrophoblast contributes to the formation of the villi but is primarily responsible for providing cells that support the syncytiotrophoblast. T/F

A

True

82
Q

Cytotrophoblast would penetrate the syncytiotrophoblast layer and form outer cytotrophoblast layer. It has primary villi, secondary villi, and teritiary villi. The villous cytotrophoblast cell is a type of cell found within the chorionic villi (created by syncytiotrophoblast) of the placenta. FYI: the blood vessels are also located in the chorionic villi. T/F

A

True

83
Q

Bones are not fully mineralized until about 2 years old. T/F

A

True

84
Q

Decrease in progesterone needs to happen for parturition. T/F

A

True

85
Q

Oxytocin relies on positive feedback loop. T/F

A

True

86
Q

In mother, cortisol inhibits hypothalamic CRH & pituitary ACTH release, creating negative feedback loop. T/F

A

True

87
Q

CRH is stimulated by cortisol from the decidua, trophoblast, fetal membranes, creating positive feedback loop for both the mother & fetus. T/F

A

True

87
Q

Maternal CRH increases even as fetal CRH decreases due to cortisol feedback. T/F

A

True

88
Q

Role of elevated cortisol from stimulating CRH in pregnancy:

A

Changes in estrogen & progesterone ratios that prepare the body for labor.

Myometrial contractility, relaxation or contractility depending on receptor.

Inflammation in myometrium

Fetal adrenal function, lung maturation, & surfactant production

89
Q

Oxytocin is a polypeptide hormone? T/F

A

True

90
Q

What produce oxytocin:

A

Maternal hypothalamus (posterior pituitary)

Uterine contraction

Placenta & decidua to produce prostaglandins

91
Q

Prostaglandins are cyclic fatty acids, PGF2a & PGE2, and stimulate uterine contraction? T/F

A

True

91
Q

What produces prostaglandins?

A

Placenta & uterine tissue

92
Q

Estrogen from ovaries induces oxytocin receptors on uterus: T/F

A

True

93
Q

CRH are neuropeptide produced by the hypothalamus, maternal & fetal brain, placenta? T/F

A

True

94
Q

Important component of HPA axis:

A

Can be activated by stress

95
Q

Action of produced glucocorticoids:

A

High estrogen production
High prostaglandin synthesis

96
Q

Placental estrogen induce synthesis of prostaglandins, and its production in chorion and amnion cells. T/F

A

True

96
Q

the potential for fetal cortisol negative feedback action on fetal ACTH production is reduced by increased production of corticosteroid-binding globulin (CBG) at the end of pregnancy. T/F

A

True

97
Q

Placental estrogens enhance placental CRH production, second positive feedback loop? T/F

A

True

98
Q

Placental CRH synthesis is stimulated by fetal cortisol (positive feedbackloop): T/F

A

True

99
Q

Rotate the baby to prevent head or skull deformation: T/F

A

True

100
Q

Fetal Health Metrics or good prenatal care assessments:

A

Maternal weight gain

M cardiovascular adaptation

Insulin requirements

Fetal growth profiles

Genetic screening (no injection of needless to prevent risk of infection) ultrasound scanner

Placental health

Uterine, placental. and umbilical blood flow

101
Q

Pregnancy hormones & their effects:

A

Estrogen, cortisol, human placental lactogen can have blocking effect on insulin.

102
Q

Our insulin needs start to increase from when you are 20 weeks pregnant. Eventually, you may need 2 or 3 times the amount of insulin that you had before you were pregnant.
T/F

A

True

103
Q

How to counteract the blocking effect of these pregnancy hormones:

A

Need more insulin for food to pass into your own body cells (and feed the fetus)

104
Q

Neonatal health metrics at birth:

A

Gestational age at delivery
Mode of delivery
Birthweight centile
Neonatal biometrics
Neonatal organ function
Feeding behaviors
NICU Admission

105
Q

Complications and pregnancy outcomes

A

Infertility and miscarriages
Ectopic pregnancies
Pre-term Birth
Placenta-Mediated Disease
Placenta previa
Placenta accreta
Molar pregnancies
Fetal growth restriction (FGR/IUGR)
Preeclampsia
Gestational Diabetes *
Stillbirth*

*significant

106
Q

What is one of the causing of pre-term birth.

A

The woman not knowing that she is pregnant and leads to poor prenatal care.

107
Q

Birth <37 weeks gestation is pre-term birth and early pre-term birth is <32-34 weeks.

A

Yes

108
Q

More than 90% of pre-term birth survive. T/F

A

True

109
Q

Causes of pre-term births:

A

Stress, systemic material genital tract infections, placental ischemia, or vascular lesions, & uterine contraction.

This lungs are not well-developed.

110
Q

What makes pre-term birth have increased morbidity & adult chronic disease:

A

Hypertension
Cardiac dysfunction
Lung disease
glucose intolerence
Developmental programming are missed

111
Q

What is impaired intrauterine fetal growth:

A

Fetal growth restriction (10th, 5th, 1th percentiles)

112
Q

Characteristics of FGR:

A

IUGR/FGR - did not reach full growth (abnormal uterine and/or umbilical artery blood flow) due to issues with the placenta.

SGS - small compared to normal distribution. may not be pathological.

10% of births in Canada

113
Q

Ethology of IUGR:

A

Maternal factors, placental & cord abnormalities, fetal malformations

infection, malaria, chromosomal abnormalities, etc.

113
Q

Pre-eclampsia is an hypertensive disorder (placental issue not mother’s health issue but affects the mother not the fetus) with placental origin: T/F

A

True

114
Q

Leading cause of maternal and fetal mortality & morbidity.

1/2o pregnancies

A

Pre-eclampsia

115
Q

Can lead to eclampsia (maternal seizures). T/F

A

True

116
Q

S&S of pre-eclampsia:

A

Hypertension after 20 weeks gestaition

Systolic >140 mmHg or diastolic >80 mmHg

Proteinuria
Edema
Abnormal liver function
HELP syndrome

117
Q

Pre-eclampsia has no cure.

A

Yes

but delivery of placenta

118
Q

When the placenta cannot meet the fetal demands, the mother may develop hypertension as her body attempts to compensate for the inadequate placental function. This cycle can lead to further complications for both the mother and the fetus. T/F

A

True

119
Q

Etiology of pre-eclampsia:

A

Placental hypoxia and damage

Excessive shedding of placental debris in maternal circulation

Maternal inflammation and endothelial dysfunction

120
Q

Pre-term birth & FGR are common occurences: T/F

A

True

121
Q

Pre-eclampsia associated with cardiovascular & metabolic diseases in later life of offspring. T/F

A

True

122
Q

Two-hit combination of pre-eclampsia:

A

immunomodulatory and antiangiogenic signals (mid to late gestation)

later host susceptibility marked by unhealthy lifestyle

123
Q

Pregnancy predicts long-term health risk for mothers:

A

yes

124
Q

After preeclampsia, women have an increased risk of vascular disease. T/F

A

True

125
Q

Diabetes mellitus associated with pregnancy. T/F

A

true

126
Q

Majority of mother snot diabetic before pregnancy, but often goes away after pregnancy?

A

True

127
Q

Inability to produce insulin secretion to compensate for pregnancy induced insulin resistance - hyperglycemia. Dangerous for mother and fetus.

A

GD

128
Q

GD affects upto 26% of pregnancies:

A

Yes

129
Q

Risk factors of GD:

A

Advanced maternal age

Smoking

Obesity

130
Q
A