Treating depression with antidepressants | Mental health | NCLEX-RN | Khan Academy

Treating depression with antidepressants | Mental health | NCLEX-RN | Khan Academy


– [Voiceover] One popular
way to treat depression is with antidepressants, and these are drugs that help to relieve the
symptoms of depression. But before I talk about
them, I want to quickly go over neurotransmission. So here we have a neuron, and neurons receive messages
through their dendrites, which are these branching structures here. Then that electrical signal
is sent down the axon to the axon terminals at the end. Here it meets up with the dendrites of the next neuron down the line. But these cells aren’t really touching, and the electrical signal,
the action potential, it can’t actually jump
between these cells. So how does the message get
from one cell to the next? When the action potential
reaches the axon terminal, the electrical signal is actually changed into a chemical signal,
and here’s how it works. The action potential triggers the cell to release vesicles full of chemicals called neurotransmitters,
and the vesicles, these kind of cellular sacs, they dock with the cellular membrane and the neurotransmitter
spills out into the synapse, which is what we call the
space between these two cells. Once there the
neurotransmitters bump around, and they can dock onto
receptors on the next cell. When they do, this triggers
an electrical signal in that next cell. The antidepressants that we are going to be talking about today work
on this synaptic level, as do many other medications. Because by increasing
or decreasing the amount of available neurotransmitter
in the synapse, medications can make
it more or less likely that a message will be
triggered in the next cell. Depression itself seems
to work on this level. Studies have suggested
that depression might be caused by low levels of
certain neurotransmitters called monoamine neurotransmitters. This includes serotonin, norepinephrine, epinephrine, and dopamine. Different theories disagree
about the relative contributions of each one, but this
is something I want you to keep in mind when we talk about how these medications work, because all of the antidepressants
we’re going to cover in this video work by trying
to correct this imbalance. They all cause an increase in the levels of these neurotransmitters, but they do it using very different mechanisms. We’re going to cover three
classes of antidepressants, monoamine oxidase inhibitors, or MAOIs, tricyclic antidepressants, or TCAs, and selective serotonin
reuptake inhibitors, or SSRIs. So let’s start off with these MAOIs. The clue to how these
antidepressants work is in the name. Monoamine oxidase is an
enzyme that breaks down neurotransmitters that
isn’t stored in vesicles. So it’s kind of like
cellular housekeeping. Monoamine oxidase inhibitors are drugs that inhibit the actions
of monoamine oxidase. By inhibiting this enzyme,
it actually increases the amount of neurotransmitter
that is capable of being released into the synapse. More neurotransmitters
in the synapse increases the likelihood that they will dock onto the postsynaptic cell and
cause an action potential. The next type of antidepressants are tricyclic antidepressants. instead of being named for what they do, these drugs are named for how they look. I have a few examples
here, and you can tell that all of them have
this three-ring structure. So tri for three and cyclic for the rings. Tricyclics work by increasing the levels of two specific neurotransmitters, norepinephrine and serotonin. But the way that they do this
is very different from MAOIs. Instead of stopping an
enzyme from breaking down these neurotransmitters,
TCAs work by interfering with a very different
housekeeping mechanism called reuptake. Much like you, your body likes to recycle. It likes to be efficient. This is even true at the neuronal level. After the neurotransmitter
has released into the synapse, your body doesn’t get rid of
it, instead it recycles it by taking it back up
into the presynaptic cell through these reuptake channels. Then it can be repackaged into
vesicles and released again. TCAs work by blocking
these reuptake channels. The result of this is that
the neurotransmitter stays in the synapse longer,
which then increases the likelihood that it
will dock onto a receptor on the postsynaptic cell and
trigger an action potential. SSRIs, or selective serotonin
reuptake inhibitors, work the same way, they work
by blocking reuptake channels. But instead of blocking
them for both norepinephrine and serotonin like TCAs,
they only block reuptake for serotonin, and only for very specific serotonin receptors. So like MAOIs, here we have
a situation where the name of the drug is a description
of what the drug does. I think of all of these
antidepressants, SSRIs are probably the ones that you are most familiar with because this class of
drugs includes fluoxetine, which is also known as Prozac. We have three classes of antidepressants, and the question you might have is, how do doctors know
which one to prescribe? Your natural answer
might be that they should prescribe the one that works best, but it turns out that actually
all of these medications are equally effective as antidepressants. So maybe you think, okay,
if we can’t differentiate by effectiveness, maybe
we can differentiate by side effects. This is where the main differences lie. MAOIs and TCAs are the
oldest antidepressants. They are what we call “first
generation” antidepressants. But because they are the
oldest, they tend to have more side effects than more
recent drugs like SSRIs, which are considered to be a
second class antidepressant. MAOIs in particular are
notorious for having a lot of side effects, and
this stems from the fact that MAOIs affect a lot
of different things. Remember we said that they affect all of the monoamine neurotransmitters, but we also have to
remember that these drugs don’t just increase
available neurotransmitters in the brain, they do it
in the entire body as well. This can cause a lot of
different side effects. For example, MAOIs wind
up inhibiting a process in the liver that helps
to metabolize medications. As a result, people taking them need to be very careful when
taking other prescription and non-prescription medications. This is something that you
might have been aware of if you have ever paid
attention to drug commercials. Many of them note things
like people taking MAOIs should not take drug “X”,
or talk to your doctor if you are taking MAOIs. The reason behind this is
that if your body can’t break down certain drugs, it might lead to a dangerous buildup of
those drugs in your body, which could potentially
be life-threatening. But MAOIs don’t just prevent the breakdown of certain medications,
they prevent the breakdown of certain foods as well. I don’t want to get too much into this, but I would definitely
recommend that you Google the list of foods that
people on MAOIs can’t eat, because it is pretty long. It includes all fruits,
alcohols, dairy, some meats. The list is very long,
and actually the diet can be so restrictive that
people sometimes stop taking the medication. Because of these side
effects, MAOIs are no longer a popular choice for treating depression, although they are still
used when an individual has not benefited from other treatments. Before when we talked about TCAs we noticed that instead working on all of the monoamine
neurotransmitters like MAOIs, we said that they only
work on two of them, norepinephrine and serotonin. Because they are more
specific in what they affect, they also have fewer side effects. However, for some
individuals the side effects that they do have can be severe. TCAs can sometimes affect things aside from norepinephrine and serotonin, things like histamines. This can lead to fatigue and sluggishness. Another problem is toxicity. TCAs are very toxic at higher levels and someone could go into cardiac arrrest if they accidentally or
purposefully overdose on them. So individuals taking TCAS
need to be carefully monitored by doctors, especially
individuals who might be at a higher risk for suicide. Like MAOIs, the severity
of these side effects make it so that TCAs are
not always the first choice when prescribing antidepressants, although they are prescribed
when people aren’t successful with other treatments. They are also prescribed for individuals with bipolar disorder,
along with other medications like Lithium, and this is because other antidepressants, specifically SSRIs, can sometimes trigger manic episodes in people with bipolar disorder. So TCAs are generally a safer option. But this brings us to SSRIs. With the exception of very specific cases like bipolar disorder, this
class of antidepressants are generally the first
choice for individuals seeking treatment for depression. This is because they are really effective, like the other antidepressants,
but also because they have fewer side effects. This has to do with the fact that they are the most selective in what they act on. But like the other antidepressants, they aren’t side effect
free, because they also work everywhere in our brain and our body. So there are some side
effects, and these can include sleeping problems, weight
gain, and sexual dysfunctions. While these are not
life-threatening, these side effects could have a negative impact
on a person’s quality of life. There is one exception to
this life-threatening clause though, and that’s a condition
called serotonin syndrome. This rarely occurs for
people who are taking SSRIs on their own, but it can become a problem if they are combined with other substances that also increase serotonin. I’ve talked about these three
classes of antidepressants, but there are other newer substances that are also on the market now. Some of them are combined SSRIs and SNRIs, so they block reuptake for both serotonin and norepinephrine, but
only for very specific types of each, so I generally
like to think about them as more restrictive TCAs. They get all of the benefits of TCAs with fewer side effects. Another new kind of
antidepressants are NDRIs, norepinephrine and dopamine
reuptake inhibitors. Also NDRAs, norepinephrine
and dopamine releasing agents. One blocks reuptake of
norepinephrine and dopamine, and the other triggers additional
release of norepinephrine and dopamine, but both
result in an increase of these neurotransmitters in the synapse. Both of these drugs are really promising. I’m sure that they’ll only
increase in popularity as time goes on, but I really wanted to mention them here because I think that they challenge our
cultural narrative of depression being caused by a decreased
level of serotonin because these drugs relieve
the symptoms of depression without influencing
serotonin levels at all. That’s just something to keep in mind because as our knowledge
of this topic increases, how we think about depression
from both a medical and cultural standpoint
will change as well.

16 comments

  1. I've been researching reducing depression quickly and found an awesome resource at Sebs Shy Remedy (google it if you're interested)

  2. There are several things you can try
    Find the reasons why you suffer from depression – the first step in solving a problem is understanding why you have it.
    Be at ease about yourself – this makes it less difficult
    Just do it – you will feel better by taking action – especially by doing activities that stretch your boundaries.
    (I learned these and more ideas from Martos magic method site )

  3. https://youtu.be/xgsbxmiPOrg?t=98
    "Studies have suggested that depression might be caused by low levels of neurotransmitters…"
    No.  This has been known to be wrong since the 1960's and you won't find any studies that show what a normal level of monoamines is because you cannot measure high/low/or normal levels in the brain.  We simply do not know, but don't accept the marketing talk of pharmaceutical commercials as accepted and valid hypotheses.  Stick to the science.

  4. Shame shame shame khan academy. Thought you would be more scientific than jumping on the band wagon of the bullshit chemical imbalance theory. I will now unsubscribe because you are as ignorant as the rest of the psychiatric community. Shame on you.

  5. Recent evidence revealed that antidepressant pills increase suicide risks by 2-5 times. [a][b][c][d][e][h]
    Cognitive behavioural therapy halves the risk of repeated suicide attempts. [k]
    Furthermore, antidepressants increased all cause mortality by 33%! [i][j]
    Another meta-analysis published in the British Journal of Psychiatry has found that even patients with the most severe depression can expect to get as much benefit from cognitive behavioural therapy (CBT) as those with less severe symptoms. [f]
    Even Behavioural Activation effectively decreases depressive symptoms. [g]
    Trained grandmothers are better than psychiatrists.
    References
    [a] http://journals.sagepub.com/doi/pdf/10.1177/0141076816666805
    [b] http://www.bmj.com/content/348/bmj.g3510
    [c] http://www.bmj.com/content/352/bmj.i65
    [d] http://nordic.cochrane.org/sites/nordic.cochrane.org/files/public/uploads/theses/Emma%20Maund%20PhD%20thesis.pdf
    [e] http://www.bmj.com/content/355/bmj.i6103
    [f] http://bjp.rcpsych.org/content/210/3/190.long
    [g] http://www.bmj.com/content/356/bmj.j914
    [h] http://www.bmj.com/content/358/bmj.j3697/rr-4
    [i] https://brighterworld.mcmaster.ca/articles/antidepressants-associated-with-significantly-elevated-risk-of-death-researchers-find/
    [j] https://www.ncbi.nlm.nih.gov/pubmed/28903117
    [k] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650127/

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