What are the major steps in embryonic development?

Fertilization
Blastocyst Development
Blastocyst Implantation
Embryo Development
Fetal Development -12th week of development

Following fertilization, the blastocyst (which is a cluster of cells that had begun to divide
following fertilization) implants itself in the uterine lining through the trophoblast cells (help with
the attachment of the blastocyst and eventually become a part of placenta). This process of
implantation has a high fail rate, from 50% to 75%, explaining why a successful pregnancy
typically requires several attempts to achieve.

The fusion of the trophoblastic cells then creates syncytiotrophoblast (a collection of

specialized cells that fuse to the uterus lining in order to attach the blastocyst to its wall). This
structure then secretes the human chorionic gonadotropin (hCG), a hormone that stimulates
the corpus luteum to enlarge and continue producing progesterone, thus preventing the process
of menses from happening during pregnancy. The process of implantation is completed by the
middle of second week, resulting in high enough levels of hCG to be detected in urine tests.

During the second week of development, the blastocyst begins to organize itself in
layers. The amniotic cavity is formed (a two layered disc of embryonic cells formed from the
blastocyst that opens up between it and the trophoblasts). Cells from the upper layer of the disc
(the epiblast) extend around the amniotic cavity, creating a membranous sac that forms into the
amnion (innermost membrane that encloses the embryo) by the end of the second week. This
sac is then filled with amniotic fluid, which serves to protect the embryo from physical trauma as
well as filter out waste such as urine.

On the ventral side (inner side) of the embryonic disc, opposite of the amnion, cells in
the lower layer of the embryonic disk (the hypoblast) extend into the blastocyst cavity and form
a yolk sac, which then supplies nutrients to the growing fetus. As the baby continues to develop,
the placenta that connects it to the mother provides it with further nutrients and oxygen for
healthy growth all the way up until labor.

The studies and the Sources

Cocaine is an excitatory drug that causes increased alertness and energy and reduced
fatigue. These effects result from the increased activity within several neurotransmitter systems,
primarily dopamine. Cocaine reduces the reuptake of the neurotransmitter, leading to its
excitatory effects on the body. The use of the drug during pregnancy can lead to premature
birth, low birth weight, and miscarriage, all of which are linked to increased blood tension. Even
the post-pregnancy use of the drug leads to complications within the child such as tachycardia,
seizures, and hypertension.
 I decided to talk about the impacts on the babies that cocaine has if used during
pregnancy. Strictly speaking it is a chemical cause - the diffusion of the drug through the
placenta into the fetus has long lasting effects post birth. However, there are direct and indirect
impacts, direct where the baby is directly impacted by the drug, and indirect where the
complications that arise with cocaine impact the mother, which then impairs the development of
the fetus. It is also important to underline that the effects of cocaine cannot be traced to a
specific stage of fetal development, the fetus is being affected by the drug throughout its
development, but even a single dose can have hindering effects on the proper developmental
cycle.

The indirect effects of cocaine typically result from the changes in the mother’s Central
Nervous System (CNS). The indirect danger that cocaine poses to a developing fetus is the
impairment of the blood flow to the uterus, which causes an undersupply in oxygen due to
elevated catecholamine levels (types of neurotransmitters such as dopamine) and placental
vasoconstriction. This is because cocaine blocks the reuptake of catecholamines, a hormone
that causes vasoconstriction, leading to more constriction in the uterine blood vessels. This
typically comorbiditizises with other heart conditions, which could lead to premature birth. The
undersupply in oxygen leads to irreversible damage in the fetus as the tissues develop at a
delayed rate.

The direct effects of cocaine are linked to the drug’s transfer through the placenta,
leading to alterations in synaptic transmission. The drug blocks the presynaptic reuptake of the
neurotransmitters norepinephrine and dopamine, producing an excess of transmitter at the
postsynaptic receptor sites. These effects, in the same venue as the indirect effects, lead to
vasoconstriction, also leading to the development of tachycardia, and a rise in the arterial blood
pressure.

In both cases, the results of vasoconstriction, tachycardia, and increased blood pressure
leads to intermittent intrauterine hypoxia, preterm labour, precipitous labour, and abruptio
placenta (placenta separates from the wall before birth), followed by hemorrhage, shock, and
anemia. Approximately 25% of the offspring from mothers abusing cocaine display these traits.

The study that I was looking over analyzed the effects of vascular hypertension through
the frequency of the baby’s cry, attempting to correlate a mother’s abuse of cocaine to a child’s
underdevelopment. It was hypothesized by the researchers that cocaine could affect excitable
cry characteristics independent of the mediating effects of IUGR (intrauterine growth retardation)
through direct factors, whereas the effects of cocaine on depressed cry characteristics would be
mediated by IUGR through indirect factors. Excitable characteristics included the reduced time it
took the infant to respond to the stimulus and the longer duration of the cry, while the depressed
characteristics included lower amplitude of the sound, and a longer latency. The researchers
believed that both factors emerged as a result of an impaired CNS of the children.
 The results of the study revealed that the cocaine-exposed infants had a significantly
lower birth weight, shorter birth length, and smaller head circumference than the control group.
The direct effects showed that cocaine use was linked to cries longer in duration and cries with
a higher fundamental frequency, which were linked to the drug and not the reduced birth weight.
These effects are linked to increased respiratory effort, increased laryngeal tension, and
constriction of the upper airway. The indirect effects were linked to longer latency from stimulus
application to cry onset as well as a lower amplitude of the cry, which were linked to both the
drug and the reduced weight of the children. These effects as opposed to the direct effects were
linked to a hyporesponsive CNS with consequent poor respiratory effort.

A child who was affected by this disorder may be born addicted to cocaine as well as
have other physical deformities, although not as often as with other disorders such as the fetal
alcohol syndrome. Impaired growth can further limit the proper development of the child,
however with proper attention and care the child can live a life similar to non-affected
individuals. Most often than not however, these children are born into dysfunctional families,
which frequently abuse them, compounded by the use of cocaine by other family members.