WEBVTT

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All right, so today we're gonna
be talking about antidepressants. Thank you everybody

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who's supporting the podcast, the really
nice comments, everything, I really appreciate

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it, and thank you so much
for today's sponsor, True Learn. So

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let's talk about antidepressants, SSRIs,
S, NRIs, TCAs MAOIs, atypical

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antidepressants. There's a lot to know
here, so I'll keep it as high

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yield as possible and throwing a bunch
of nomonics to help you remember what you

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really need to know. Before we
get started, let's really quickly talk about

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a couple basic fundamental concepts that will
help you better understand the meds will go

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over today. Let's start with the
monoimmine hypothesis. So the monomine pothesis dates

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back to the nineteen fifties, basically
states that the underlying pathiophysiologic basis of depression

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is essentially a depletion in levels of
serotonin or apenephrine or dopamine in the CNS.

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Now, we've learned a lot over
the years and we know that's not

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all that's going on. There's definitely
more to it than just a chemical imbalance.

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But understanding this basic concept, it's
going to help you better understand the

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meds will go over today and their
propose mechanism of action. So before we

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start with the first class of meds, let's really quickly run down this whole

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neuro transmitter exchange in the brain.
So we have two neurons close together.

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One neuron is the presynaptic neuron,
the other is the post synaptic neuron.

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They're separated by a teeny tiny space
called a synaptic left. So the presynaptic

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neuron, it's got all the goodies
depending on which type of neuron we're referring

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to, serotonergic et cetera. It's
stocked with either dopamine, serotonin, neuropinephrin,

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and they're all stored in these sac
like structures called vesicles. So eventually

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we have to get those neurotransmitters out
of those vesicles so they can do their

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work. So what happens is an
action potential zaps this presynaptic neuron, which

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causes these vesicles to open up and
dump their delicious contents into that presynaptic left

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between the two neurons. At this
point, those neurotransmitters dopamine, serotonin,

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et cetera. They bind to the
receptors on the post synaptic neuron and then

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they work their magic. After a
period of time, though the neurotransmitters that

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are still hanging out in the synaptic
left not really doing much. Bodies got

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to clean them up. So some
of them will just drift off in a

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process called diffusion. Other cases they'll
be sucked back into that presynaptic neuron and

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potentially broken down by an enzyme not
as monoamineoxidase. A lot of the meds

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will go over today impact this specific
area inhibiting that clean up process. Some

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meds block the reabsorption of those neurotransmitters, allowing them to hang out in the

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synaptic left for longer. Some meds
block monominoxidase, so those neuro transmitters aren't

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broken down. It can be recycled
for another go. And we'll dive deeper

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into that once we break down each
individual class of medication. So that's the

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basics. Now that we have that
covered, we'll get started and we'll start

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with arguably the most important class of
medication to know for psych and that's your

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SSRIs, our selective serotonin reuptake inhibitors. If you're going to focus on one

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class of medication for psych Let it
be SSRIs. You get a question and

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it says, which is the first
line med for the psychiatric disorder? And

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you can't remember which met it is? Pick an SSRI and you got to

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good chance of getting it right.
So the meds in this class are cytalopram

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esketalaprem, fluoxetine, fluvoxamine, roxetine, and sertraline. It's a lot of

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weird and similar sounding meds. A
lot of these antidepressants are just really difficult

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to memorize as they all sound so
similar, and usually I don't recommend taking

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the time, but for SSRISE,
this would be the one time where I

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would make an effort if you can, because they come up so often and

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it's good to be familiar with them, so if you do want a way

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to memorize them, I do have
anemoonic. So when you think of SSRIs,

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I want you to visualize, for
now on, is a snake charmer,

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those guys who play that flute that
makes the snake come out of those

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little baskets. That's what you're gonna
associate with SSRI medications from now on.

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Think of a snake charmer. Sitting
down. He's got a parrot on his

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shoulder. Oddly enough, he's playing
the flute, and the snake also known

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as a serpent, is slowly escaping
the basket. Again, snake charmers sitting

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down, parad on his shoulder,
playing his flute. The serpent is escaping

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the basket. So sitting down should
help you remember sit talipram not the same

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spelling, but same pronunciation. Parrot
should help you remember paroxetine. And the

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parad on his shoulder, by the
way, is really fat because peroxetine is

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the SSRI associated with the most weight
gain of all of the SSRIs. And

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he's playing as flute. Flute helps
you remember fluoxetine and fluvoxamine. And then

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the escaping serpent. Remember serpent slowly
escaping the basket. Escaping helps you remember

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escitelepram m. Serpent helps you remember
certraline. All right, hopefully that helps

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remember snake charmer every time you hear
about SSRIs. Now that we know the

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meds that are in this class,
let's talk about how they work. Well.

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The name certainly helps with that.
SSRI stands for selective serotonin reuptake inhibitor,

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so SSRIs selectively inhibit the reuptake of
serotonin. So let's start with the

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words selective, because that's actually really
important. This class of medication has relative

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little affinity for other types of receptors
besides serotonin, unlike some of the other

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meds will go over today that target
a bunch of other areas, often causing

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a number of unwanted side effects.
The selectivity of this class, it's part

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of the reason they're so well tolerated
and have a relatively benign side effect profile.

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It's also the reason they're preferred over
other classes quite often. Select Ativity

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definitely important. Now, how do
they inhibit the reuptake of serotonin? Why

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does this matter? But we talked
about this briefly before. So SSRIs do

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this by decreasing the action of that
presynaptic reuptake pump, that pre synaptic serotonin

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reuptake pump, So they essentially block
the removal of serotonin from the synaptic left

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for a period of time. It's
like if there was a big vacuum sucking

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up all the serotonin from the synapse. SSRIs just come in and plug that

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up, so in turn, we
have more serotonin hanging around for longer and

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it was originally hypothesized that more serotonin
meant improved mood, and that's how these

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meds work, and it was so
simple, but in actuality, it's not

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that simple, and we later realized
there's more to it than that, because

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if the effect of SSRIs were solely
based on the fact that they just inhibit

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reuptake of serotonin leading to increased serotonin
levels, they'd be effected from day one,

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as serotonin levels increase very rapidly after
taking the first dose. But in

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actuality, the full therapeutic effect of
SSRIs usually takes many weeks to manifest,

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so we know something else is going
on here besides the increased serotinergic activity.

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And I don't think you need to
know this for your exam, but it's

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believed SSRIs also increase production of neuroprotective
proteins that can modify serotonergic receptors, and

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these added effects, which occur in
the week's following initiation of the medication,

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are thought to be the reason for
the delay therapeutic benefit. So for the

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exam, remember, these drugs selectively
inhibit reuptake of serotonin, leading to increased

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serotonin activity in the CNS. But
for real life. Realize there's more to

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it than that. All right,
Now, let's talk about the indications for

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these meds next. Starting with major
depressive disorder unipolar major depressive disorder, so

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when we're talking about pharmacologic therapy for
treatment of depression, SSRIs are usually going

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to be your first line agents.
Now, depending on the comorbidities the patient

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has, in some cases snrize atypical
an adepressants and serotoninodulators that will go over

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later, they can be reasonable alternatives
to ssriz for initial treatment, but in

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general most patients you're going to start
with an SSRI. So some other indications

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for SSRIs are generalized anxiety disorder,
panic disorder, post traumatic stress disorder,

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pre menstrual syndrome, and pre menstrual
dysphoric disorder, obsessive compulsive disorder, and

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then blimia nervosa, but specifically fluoxetine, so believe me is another indication for

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SSRIs. Specifically fluoxetine though, is
what you should remember as it's the only

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FDA approved med Other SSRIs can be
you second line, but the only f

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first line FDA proved met for bolimia
is fluoxetine. So this is such an

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easy test question. I know I
got it, and you'll probably be asked

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this, so how can you remember
this? I have a mnemonic. It's

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not perfect, but it's going to
at least help you down narrow down the

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choices on an exam question. So, bolimia has the word bull in it,

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so a bull is a cow with
horns, and then fluoxetine has the

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word ox in it, and then
ox is just another type of caw with

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horns. So when you see bulimia, think of an ox as in fluoxetine,

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the other caw with horns bolimia,
fluoxetine, bull and an ox.

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The only crappy part about this mneumonic
is there's other meds in this class that

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have the word ox in them,
peroxetine, fluvoxamine, but the rest of

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the SSRIs do not, and a
lot of the other classes don't. So

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it's going to at least help you
narrow it down on the answer choices.

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So they ask you what's your first
line med for bulimia, be thinking of

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a bowl, then remember your other
cow with horns and ox, and then

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make sure you look for a med
with the word ox in it. And

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then you can narrow it down that
way. So there's some other indications,

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but those are the main ones you'll
likely be tested on, and that's what

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you should be aware of. Let's
next move on to our adverse effects.

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So, because SSRIs are so selective, as we discussed before, mainly just

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affecting the serotonin receptor and not messing
around with the other stuff like the cholinergic

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receptors exception being proxyetine. Anyways,
because of the selectivity, they have a

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relatively benign side effect profile. With
that being said, they still of course

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have some side effects. So which
ones do you need to know for the

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exam. Let's start, of course
with the black box warning, as you

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should always know any block box warning
for any medication class. So SSRIs increase

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the risk of suicidal ideation in children, adolescents, and adults younger than twenty

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five years. This doesn't seem to
be the case for older adults, but

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patients twenty four and under need to
be aware of this black box warning.

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Now, this black box warning isn't
just for SSRIs. In two thousand and

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four, the FDA issued this black
box warning for all antidepressant drug classes SSRIs,

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SNRIs, TCAs, etc. So
this isn't unique to SSRIs, and

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I'm not going to bring this up
every single med class we go over for

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the sake of time. But just
be aware of this risk with all antidepressants,

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all right. Next is QT prolongation, specifically citalopram most importantly, and

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then esctalopram. This is a very
important one when it comes to QT interval

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prolongation. The biggest culprit by far
is citalopram. You need to know cetalobram

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can cause QT interval prolongation. Esctalopram
it's a close second. Studies are not

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as convincing. And then the other
SSRIs in the class have minimal to no

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impact on QT interval. So you
need to know these two, especially citalopram.

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They're going to ask you this at
some point on an exam question.

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So when you see an exam question
that asks which SSRI should be avoided in

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a payd with long QT syndrome,
I want you to think of this sentence.

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If you long for quiet time,
you need to escape the city.

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If you long for quiet time,
you need to escape the city. Long

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for quiet time helps remember long QT
quiet time QT long for quiet time,

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long QT escape helps remember escitalopram,
and city helps you remember the most important

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of all, citalopram. So again, if you long for quiet time,

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you need to escape the city.
That's going to help you remember. The

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SSRIs associated with prolongation of the QT
interval citalopram and esctelepram. Sexual dysfunction is

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another one. It's one of the
most common adverse effects of SSRIs. Actually,

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it's been estimated that sexual appairment and
roughly fifty percent of patients treated with

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SSRIs. This occurs in both men
and women and includes decreased libido, decreased

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arousal, delayed orgasm. Sometimes this
will get better as the weeks go on

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if they've been taking the SSRI for
a while. Sometimes you need to decrease

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the dose to kind of help with
this. Sometimes you just need to change

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the metal together. In some cases
though, the side effects are actually beneficial.

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For instance, SSRIs are considered first
line treatment for men with premature ejaculation.

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So sexual dysfunction another big one you
need to know. And then serotonin

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syndrome. It's a potentially lethal condition
that usually results from an interaction between multiple

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meds that increase serotenergic neurotransmission. It's
not specific to SSRIs, as this can

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be caused by pretty much all the
antidepressants will go over today all of the

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serotonergic agents. But SSRIs are one
of the more commonly implicated groups of meds

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leading to serotonin syndrome, probably because
their frequency of being prescribed. They're so

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commonly used and they're usually associated with
a more benign course though compared to other

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classes like MAOIs, which can often
be fatal with serotonin syndrome. And we'll

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talk about more about that later once
we get into that class. Next,

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hyponatremia, So SSRIs are also associated
with SIADH and hyponatremia. The risk is

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pretty low, but you want to
be careful prescribing to these patients who are

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at risk for hyponatremia, your older
patients, patients taking diuretics, et cetera.

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And then finally we have weight changes, so SSRIs can be associated with

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weight gain. It's usually not a
significant amount of weight, and sometimes it's

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not clear whether it was caused from
the med or the weight gain was just

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the result of recovery from depression.
But it is possible to see some weightain

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with the ssrise Fluoxetine usually causes the
least amount of weight gain, and then

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peroxetine usually causes the most weight gain. Remember the fat parrot to help your

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remember. Peroxytine causes the most weake
in of the SSRISE. Now there's other

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adverse drug reactions nausea, headache,
insomnia, bleeding, but for the exam,

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the ones that went over those are
the ones that are likely to be

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tested on, So focus on those
all right. Next class is our SNRIs

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serotonin nor epinephrine reuptake inhibitors. This
includes ben lefaccine, deuloxetine, level,

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manaciprim, milnacipran, and ben lefaccine. So there's five meds in this class,

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but if we're being real for an
exam, I just focus on two,

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deloxetine and ven lafacxine. Know those
really well, especially deloxetine, that's

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likely what you'll be tested on.
As far as the mechanism of action,

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they block presynaptic reuptake of serotonin and
nor epinephrin, so very similar to SSRIs.

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SNRIZE inhibit the reuptake of serotonin,
but they also inhibit the reuptake of

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norepinephrin. They do this by binding
two and inhibiting the serotonin and norepinephrin transporters

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on the serotonergic and neuadrienergic neurons.
They're also technically weak inhibitors of dopamine reuptake,

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but the effect is pretty minimal and
I wouldn't worry about that. Main

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effect is on serotonin and nor epi. Now you probably don't need to know

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this, but how well these meds
affect nor epinephrin or serotonin really depends on

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the drug and the dose. For
instance, venlofaxine at low doses is essentially

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just an SSRI It really just affects
serotonin, whereas in high doses of ventlefacxine

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it has really significant effects on norepinephrin. So it's just a little extra knowledge.

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So again, with SSRIs we were
really just affecting one neurotransmitter, serotonin.

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With s nrize we have effects on
two serotonin and norapinephrim. So you'll

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notice a lot of overlap when comparing
these two classes. A lot of their

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indications out of our drug reactions are
the same, but there are some differences

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due to this new interaction with nor
epi, which will go over shortly,

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so let's talk about the indication's next
lot of overlap. Like I just talked

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about with SSRIs, so unipolar major
depressive disorder. Just like SSRIs, SNRIs

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are obviously indicated for treatment of depression. And you might wonder if a class

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that affects both serotonin and nor epi
would be more effective than SSRIs that just

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affects serotonin, And the answer is
technically yes, snrize have proven to be

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a bit more efficacious than SSRIs,
but the advantage is fairly small. And

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with that being said, SSRIs are
still usually preferred first line for depression,

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but sentrized are reasonable alternative for initial
treatment in certain patient populations, which we'll

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talk about shortly. SNRIs are also
indicated in generalized anxiety disorder, post traumatic

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stress disorder, panic disorder. So
there's a lot of similar when comparing snriz

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to SSRIs, But when things are
the same, that's usually not what's going

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00:15:05.480 --> 00:15:09.840
to be tested on. What's usually
tested on is the unique aspects and what

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makes s NRIs different than SSRIs,
and what we should really be familiar with

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is their ability to treat chronic pain
syndromes like diabetic peripheral neuropathy, fibromyalogia,

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chronic muscular skeletal pain. So snriz
possess analg sequalities that we did not see

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with the use of SSRIs, and
this is likely due to the fact that

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SNRI is also target or P.
As we discussed, this neurotransmitter likely plays

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00:15:35.639 --> 00:15:39.240
a role in some form of pain
modulation. So this is the main difference

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00:15:39.279 --> 00:15:41.519
to know for indications as the rest
are as. The rest are really just

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a repeat from SSRIs, so s
nrize, in addition to treatment of depression,

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anxiety, et cetera, also have
a dual purpose for treating chronic pain

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syndromes, so you need to remember
that. And the s NURI you really

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00:15:54.159 --> 00:15:58.960
need to know is douloxetine because while
the other SNRIs have indications for some chronic

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pain syndromes, duloxetine actually has the
largest evidence base to support nalgesic efficacy and

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it's FDA proof not only for fibromyalgia, chronic lower back pain, osteoorithritis,

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but diabetic neuropathy as well. So
that's the one you really need to know,

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00:16:14.399 --> 00:16:15.840
and that's the one they'll likely test
you on the way that you're gonna

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remember that is by instead of remembering
duloxetine, remember it as dual loxetine dul

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dual oxetine, as it's dual indicated
for both major depression as well as chronic

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pain. Then you can also remember
dual oxetine because it's a dual action agent

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00:16:33.600 --> 00:16:37.679
that has an effect on both serotonin
and norepinephrine. All right, adverse drug

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00:16:37.759 --> 00:16:42.120
reactions next. So, just like
SSRIs, s NRIZ are pretty specific,

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00:16:42.200 --> 00:16:47.519
meaning they have little to no effect
on your alpha one adrinergic receptors, your

242
00:16:47.559 --> 00:16:51.799
cholinerges, your kissamine receptors. And
because of this, like SSRIs, they

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00:16:51.799 --> 00:16:55.559
have a fairly clean side effect profile
and their side effects are pretty similar to

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00:16:55.639 --> 00:16:57.279
SSRIs, a lot of overlaps,
so I'm not gonna waste your time with

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00:16:57.360 --> 00:17:02.799
the similarities. Yes, just like
SSRIs, they can cause hyponatremia, nausea,

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00:17:03.080 --> 00:17:07.640
sexual dysfunction, serotonin syndrome, bleeding, same black box warning for increased

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00:17:07.680 --> 00:17:11.319
suicidal ideation and young adults. Well, you should really focus on in what's

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different. So we know this class
is affecting an additional neurotransmitter, nor EPI,

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So this causes new issues we didn't
see with SSRIs, the main one

250
00:17:18.480 --> 00:17:23.680
to know is hypertension. So this
one's unique. Snriz can cause hypertension,

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00:17:23.920 --> 00:17:27.319
which appears to be due to their
effect in neuropinephrin. So this is different

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00:17:27.359 --> 00:17:30.599
compared to SSRIs and this is the
one to focus on. Again, Remember

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00:17:30.599 --> 00:17:34.279
focus on those unique aspects of these
classes because there's so much to know.

254
00:17:34.599 --> 00:17:37.480
You don't want to waste your time
with the overlap. Focus on the stuff

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00:17:37.519 --> 00:17:42.559
that's different. All right, So
quick recap. Remember snrize have dual effects.

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00:17:42.559 --> 00:17:48.039
They target not only serotonin but norropinephrin. Remember they not only treat depression

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00:17:48.079 --> 00:17:52.480
but also chronic pain syndromes. Deloxetine
is the main one to know aka dual

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00:17:52.519 --> 00:17:56.480
oxetine. And for ADR's focus on
hypertension. Let's move on to our TCA's

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00:17:56.559 --> 00:18:02.200
next. All right, So tricyclic
anidepress or TCAs. These were developed back

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00:18:02.200 --> 00:18:06.559
in the nineteen fifties starting with empromine, and they became first line treatment for

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00:18:06.599 --> 00:18:10.880
close to thirty years for depression.
So why did we stop using them?

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00:18:10.920 --> 00:18:12.880
Well, it wasn't for their lack
of efficacy. It's quite the opposite,

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00:18:12.960 --> 00:18:18.480
as they wore and still are very
effective in treating depression, But the same

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00:18:18.480 --> 00:18:22.319
thing that makes them so effective,
being very broad spectrum and interacting with so

265
00:18:22.319 --> 00:18:25.880
many neurotransmitter systems, it's also the
same thing that makes them so dangerous,

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00:18:25.920 --> 00:18:30.160
as they have numerous side effects and
they have a very low threshold for overdose.

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00:18:30.440 --> 00:18:33.119
So due to this, this class
of meds has fallen out of favor

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00:18:33.359 --> 00:18:37.920
and has been replaced by newer,
safer classes like the SSRIs and SNRIs.

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00:18:37.839 --> 00:18:42.119
They still do have some utilization in
certain types of issues which will go over

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00:18:42.200 --> 00:18:45.920
later, but not so much for
depression anymore. All right, So what

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00:18:45.960 --> 00:18:48.240
meds are in this class? While
there's two main groups. TCAs are broken

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up into your tertiary TCAs they're known
as, which include amatriptoline, chlomipramine,

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doccipin, empromine, trimipramine, and
then your secondary TCAs, your secondary amens,

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00:19:00.000 --> 00:19:04.000
which are decipromine, nor trip delene, and pro triptlene. So there's

275
00:19:04.079 --> 00:19:07.559
a lot of meds in this class, and there's not a good way to

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00:19:07.599 --> 00:19:10.920
memorize all of them, and I
strongly suggest against trying to do so,

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00:19:10.960 --> 00:19:14.559
you're just gonna waste your time.
But if you want to remember one that

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00:19:14.599 --> 00:19:17.960
will likely be tested on. Remember
Emma trip Delen. And if you're feeling

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00:19:18.000 --> 00:19:19.920
a bit more ambitious and you want
to remember a few of the high old

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00:19:19.920 --> 00:19:25.079
meds in this class, just remember
you're tripping if you're thinking about prescribing a

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00:19:25.119 --> 00:19:29.240
TCA. You're trippin'. If you're
thinking about prescribing a TCA, so trippin'

282
00:19:29.359 --> 00:19:33.759
trip space Pin. If you're thinking
about prescribing a TCA, trip helps you

283
00:19:33.799 --> 00:19:38.319
remember Amma trip Delene, nor trip
Delene, pro trip to line and pin

284
00:19:38.519 --> 00:19:41.799
helps remember Doc Sipin. That's all
I remember from my exam, and it

285
00:19:41.839 --> 00:19:45.920
was enough for me to get the
question right. So remember you're tripping if

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00:19:45.920 --> 00:19:48.000
you're thinking about prescribing a TCA.
All right, so now that we know

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00:19:48.039 --> 00:19:51.440
the meds in this class, or
at least the important ones, let's talk

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00:19:51.440 --> 00:19:56.960
about how they work next. So
TCAs inhibit serotonin and nor epinephrine reuptake.

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00:19:56.160 --> 00:20:00.039
So you might be thinking that sounds
a whole lot like how NRIs worked,

290
00:20:00.039 --> 00:20:06.200
and you're right, scent arize inhibited
serotonin and orpinephrine reuptake. But the difference

291
00:20:06.480 --> 00:20:10.319
is they did this very selectively and
very precisely, kind of tiptoed in.

292
00:20:10.400 --> 00:20:12.400
Did what they needed to as to
not disturb other systems in the body,

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00:20:12.720 --> 00:20:17.240
which is why they had a very
clean side effect profile. TCA's, on

294
00:20:17.279 --> 00:20:19.200
the other hand, they come in
like a wrecking ball, not only affecting

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00:20:19.279 --> 00:20:26.200
the intended targets serotonin and norepi,
but also affecting the muscarinic receptors, histamine

296
00:20:26.200 --> 00:20:30.319
receptors as well as others, causing
a bunch of unintended side effects we did

297
00:20:30.319 --> 00:20:33.119
not see with scn ARISE. So
the difference really is about the selectivity of

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00:20:33.160 --> 00:20:38.359
this class or lack thereof. So
indications for TCAs they're not really high yield.

299
00:20:38.359 --> 00:20:41.039
I wouldn't waste a whole lot of
time here, as many other classes

300
00:20:41.119 --> 00:20:45.839
have replaced TCA's as first line agents, but sometimes these still do come up

301
00:20:45.880 --> 00:20:49.440
on exam's questions. So let's really
quickly run down through some of the indications.

302
00:20:51.000 --> 00:20:55.119
So starting with major depressive disorder,
these are not first line medser depression.

303
00:20:55.480 --> 00:20:57.119
You're not going to use a TCA
for depression. This isn't going to

304
00:20:57.119 --> 00:21:00.799
be the answer on the test.
Unless they specifically mentioned they have tried and

305
00:21:00.880 --> 00:21:06.440
failed multiple other classes SSRIs, S, centriize, et cetera. They may

306
00:21:06.480 --> 00:21:08.880
still be called tricyclic anidepressants, but
you're generally not going to use them for

307
00:21:08.960 --> 00:21:14.680
depression unless all else fails due to
their pre side effect profile. Next obsessive

308
00:21:14.680 --> 00:21:18.519
compulsive disorder, specifically clomippromine, so
clomippermine can be used for the treatment of

309
00:21:18.559 --> 00:21:22.400
OCD, but SSRIs are usually going
to be or not. Usually they're going

310
00:21:22.440 --> 00:21:26.160
to be first line. Clomippermine,
though, is another treatment option only if

311
00:21:26.279 --> 00:21:33.400
SSRIs proved to be ineffective. Diabetic
neuropathy TCAs can be used am atriptlene or

312
00:21:33.400 --> 00:21:37.920
triptlene or some common options migraine prophylaxis. Am Atriptlene is the only TCA that

313
00:21:38.039 --> 00:21:45.319
has proven efficacy for migraines insufficient data. With the other TCAs nocturnal and USIS

314
00:21:45.599 --> 00:21:49.079
aka bedwetting, you can use emippromine. It's not first lined. Desmopressin is,

315
00:21:49.079 --> 00:21:52.960
but if the child has tried and
failed other treatment options including desmopressin,

316
00:21:53.319 --> 00:21:57.440
mippermine is a second line option.
I used to remember I'm appeeing instead of

317
00:21:57.440 --> 00:22:00.799
emipramine to help me remember this indication, but you probably not even can be

318
00:22:00.839 --> 00:22:06.720
asked about this. And then finally, post trapetic neuralgia usually start with gabapentin

319
00:22:06.799 --> 00:22:11.079
or per gabbling as initial therapy,
but TCAs are a reasonable second line option.

320
00:22:11.640 --> 00:22:14.599
I'm sure you notice a trend here. These are usually going to be

321
00:22:14.759 --> 00:22:18.559
backup options indication for TCAs, they're
not really high yield. I don't think

322
00:22:18.599 --> 00:22:21.240
you should waste a lot of time
memorizing them as. In general, there's

323
00:22:21.240 --> 00:22:23.960
better mets for most of these conditions. So where you should be focusing on

324
00:22:25.000 --> 00:22:27.319
when it comes to TCAs and where
the questions will usually come from on the

325
00:22:27.359 --> 00:22:32.079
exam, is with their adverse effects. So TCAs, like we touched on

326
00:22:32.119 --> 00:22:34.519
before, they got some side effects
and the side effects that they get tested

327
00:22:34.559 --> 00:22:37.720
on a lot. So let's talk
about what you need to know and a

328
00:22:37.759 --> 00:22:41.079
little mnemonic to help you remember it. So with TCAs, I want you

329
00:22:41.119 --> 00:22:45.279
to focus on that C and TCAs
to help you remember the five c'snmonic I

330
00:22:45.279 --> 00:22:49.359
came up with. So the five
c's for adverse effects of TCAs stand for

331
00:22:49.599 --> 00:22:55.759
cardiac, QT, chubby convulsions,
and anticholinergic. So what are these meaning.

332
00:22:55.839 --> 00:22:59.359
Let's start with the first C standing
for cardiac, So all of the

333
00:22:59.400 --> 00:23:03.519
TCAs are a potentially cardiotoxic so you
want to avoid this class in susceptible individuals

334
00:23:03.559 --> 00:23:10.160
with heart disease. TCAs can slow
intracardiac conduction, cause various arrhythmias, orthostatic

335
00:23:10.240 --> 00:23:14.359
hypotension, and the most important cardiac
adverse effect that you need to remember,

336
00:23:14.519 --> 00:23:18.640
and it's so important it gets its
own C is QT QTCUTI should help your

337
00:23:18.680 --> 00:23:25.519
member QT prolongation QT QT prolongation.
So this is a major concern with TCAs,

338
00:23:25.680 --> 00:23:29.279
especially when you mix these meds with
other classes that can prolong the QT

339
00:23:29.400 --> 00:23:34.079
interval, like certain antimicrobials anti arrhythmic
drugs. QT helps your member QT prolongation.

340
00:23:34.480 --> 00:23:41.119
Next C stands for chubby straightforward.
The cyclic to antidepressants block histamine receptors,

341
00:23:41.319 --> 00:23:45.279
which can cause increased appetite leading to
weight gain. Next C very important

342
00:23:45.319 --> 00:23:48.759
one convulsions. All of the TCAs
can lower seizure threshold. This is dose

343
00:23:48.799 --> 00:23:52.599
dependent, so the higher the dose, the greater the chance of a seizure,

344
00:23:52.880 --> 00:23:56.200
especially in overdoses, so convulsions aka
seizures. And then the last C

345
00:23:56.400 --> 00:24:02.799
and one of the most important is
for anticholinar dry mouth urinary retention confusion.

346
00:24:02.880 --> 00:24:06.920
All can start from this, so
we touched on this before TCAs they're not

347
00:24:07.079 --> 00:24:11.279
very selective and they affect a number
of neurotransmitter systems. One of those is

348
00:24:11.279 --> 00:24:18.000
your muscarinic receptors. TCAs block the
muscarinic acetylcholine receptors, which causes anticholinergic effects.

349
00:24:18.200 --> 00:24:22.279
So these patients may have dry mouth, urinary retention, confusion, blurred

350
00:24:22.319 --> 00:24:26.119
vision, tachycardia, et cetera.
Just remember anticholinergic for the last c all

351
00:24:26.200 --> 00:24:29.880
right, So those are your five
SE's of TCAs that you need to know,

352
00:24:30.279 --> 00:24:33.400
cardiac qt, chubby convulsions, and
anticholinergic. If you know those,

353
00:24:33.640 --> 00:24:37.200
you should be good for the exam. Now. One last thing to be

354
00:24:37.240 --> 00:24:41.240
aware of is the potential for overdose
with TCAs. TCAs have a high potential

355
00:24:41.279 --> 00:24:45.839
for overdose, especially when we compare
them to SSRIs. For instance, take

356
00:24:45.960 --> 00:24:49.759
only takes as little as ten times
the daily dose of a TCA to be

357
00:24:49.880 --> 00:24:53.839
fatal. Compare this to an SSRI, where it usually takes a really large

358
00:24:53.880 --> 00:24:57.799
dose, usually greater than one hundred
and fifty times the daily dose to prove

359
00:24:57.839 --> 00:25:02.039
fatal. So in a PATI overdoses
on a TCA, it can lead to

360
00:25:02.079 --> 00:25:07.359
anticholinergic toxicity seizures, but most concerning
it can prolong the QT interval so you

361
00:25:07.359 --> 00:25:11.759
can give them benzos to control the
seizures. But the most important therapeutic intervention

362
00:25:11.920 --> 00:25:15.720
and the right answer on an exam
to treat a TCA overdose is going to

363
00:25:15.759 --> 00:25:21.480
be sodium bicarb Sodium bicarbonate. You
need to know this. Sodium bicarbonate is

364
00:25:21.559 --> 00:25:26.119
the standard initial therapy for a TCA
overdose with hypotension arrhythmic QT prolongation. This

365
00:25:26.200 --> 00:25:30.240
is the intervention you need to know
for TCA overdose. It's what they're going

366
00:25:30.319 --> 00:25:33.160
to ask you. So how can
you remember this? Well? You remember

367
00:25:33.400 --> 00:25:37.680
a tricycle is a small bicycle.
A tricycle is a small bicycle. Tricycle

368
00:25:37.720 --> 00:25:42.920
helps remember try cyclic and a depressant, and small bicycle helps remember sodium by

369
00:25:44.079 --> 00:25:47.880
carbonate number. If they ask you
how you're going to treat a TCA overdose,

370
00:25:48.079 --> 00:25:53.119
remember sodium bicarbonate aka a tricycle is
a small bicycle. So I wanted

371
00:25:53.160 --> 00:25:56.960
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Now back to the show. All
right, let's move on to the

384
00:26:48.319 --> 00:26:52.599
monoamine oxidase inhibitors. The MAOIs so
MAOIs, like TCA's, were one of

385
00:26:52.640 --> 00:26:57.119
the first drugs developed to treat depression. We discover this class really by accident.

386
00:26:57.160 --> 00:27:00.960
Back in the nineteen fifties, they
were trying to develop a drug to

387
00:27:00.000 --> 00:27:06.039
treat tuberculosis, a drug called iproniazid, and during the study they found other

388
00:27:06.079 --> 00:27:11.160
potential benefits outside of its intended purpose
when the patients in the study exhibited improvement

389
00:27:11.200 --> 00:27:15.119
in mood. So this med kicked
off the MAOI class, and while ipronyzid

390
00:27:15.200 --> 00:27:18.880
was later removed from the market due
to hepatotoxicity, it was replaced by the

391
00:27:18.880 --> 00:27:22.880
other meds will go over today.
In general, MAOIs like TCAs they're rarely

392
00:27:22.960 --> 00:27:26.759
used anymore because of their side effect
profile, food and drug interactions, and

393
00:27:26.839 --> 00:27:30.319
quite simply because we have better and
safer options now. In general, these

394
00:27:30.359 --> 00:27:34.079
meds are really only going to be
used where nothing else has worked. So

395
00:27:34.119 --> 00:27:41.240
the meds in this class are chrannelcipermine, isocarboxyzid, phenozene, and celegilline aka

396
00:27:41.359 --> 00:27:47.079
tips TIPS because the letters in those
medications are tips. Just a little nomonic

397
00:27:47.079 --> 00:27:48.200
to help you remember the meds in
this class. There is another one,

398
00:27:48.240 --> 00:27:52.200
meklobamide, but it's not available here
in the US, so I wouldn't really

399
00:27:52.200 --> 00:27:55.519
worry about that one. So how
do these drugs work? While they increase

400
00:27:55.640 --> 00:28:00.839
dopaminergic, ner adrenergic, and serotonergic
neurotransmission by blocking monoamine oxidase. So I

401
00:28:00.960 --> 00:28:04.920
understand how these meds work, we
first need to understand what monomine oxidase is.

402
00:28:06.319 --> 00:28:11.079
So most of the other endidepressants we
discuss so far worked by decreasing reuptake

403
00:28:11.160 --> 00:28:15.319
of the neurotransmitters serotonin or epi,
et cetera, which in turn left more

404
00:28:15.319 --> 00:28:18.880
of them hanging out in the synaptic
left to be utilized. But MAOIs they

405
00:28:18.880 --> 00:28:22.680
work differently. So once serotonin,
nor EPI or dopamine have been reabsorbed by

406
00:28:22.680 --> 00:28:27.359
those reuptake proteins, some of those
neurotransmitters get packaged into vesicles waiting for the

407
00:28:27.400 --> 00:28:30.440
next go round to be released into
the synaptic left. But a good portion

408
00:28:30.519 --> 00:28:34.920
of those neurotransmitters are actually broken down
before they get that opportunity, and they're

409
00:28:34.960 --> 00:28:38.640
broken down by an enzyme called monoamine
oxidase, and we briefly touch on this

410
00:28:38.680 --> 00:28:42.799
at the beginning. Monomine oxidase.
It's a mitochondrial enzyme. It's found in

411
00:28:42.799 --> 00:28:45.680
the brain as well as a number
of other organs, and one of its

412
00:28:45.759 --> 00:28:52.480
jobs is to inactivate or break down
dopamine, europenephrin or serotonin once they've been

413
00:28:52.519 --> 00:28:56.799
pumped back into the pre synaptic left. So the more we inhibit monomine oxidase,

414
00:28:56.880 --> 00:29:00.319
the more neurotransmitters are available for the
next go round. Now is another

415
00:29:00.359 --> 00:29:03.480
side note. There's actually two different
types of monomine oxidase, monomine oxidase A

416
00:29:03.640 --> 00:29:10.279
and monoamine oxidase B. They both
break down different neurotransmitter. Mono monomine oxidase

417
00:29:10.319 --> 00:29:14.720
A metabolizes more neurotransmitters than monomineoxidase B, and I wouldn't worry too much about

418
00:29:14.759 --> 00:29:18.799
that though. Just know that different
meds in the MAOI class can be selective

419
00:29:18.039 --> 00:29:22.000
and that they only inhibit one type
of monomine, and some are non selective,

420
00:29:22.000 --> 00:29:26.519
in which they inhibit both types of
monomine. So the non selective agents

421
00:29:26.559 --> 00:29:33.559
are isocarboxyzid phenozene and chranocipromine non selective
again, meaning they inhibit both MAO A

422
00:29:33.039 --> 00:29:37.599
and MAO B. And then we
have celegoleine, which technically can be selective

423
00:29:37.720 --> 00:29:41.480
or non selective depending on if it's
high or low dose, but for the

424
00:29:41.519 --> 00:29:45.319
sake of the exam it's best to
just know it as a selective agent.

425
00:29:45.559 --> 00:29:51.720
So celegoleine at low doses around five
to ten milligrams selectively inhibits only MAOB and

426
00:29:51.839 --> 00:29:55.079
due to this, it's not so
effective for treatment of depression, but it

427
00:29:55.119 --> 00:29:57.880
can be used in Parkinson's disease due
to its effect on dopamine. There's a

428
00:29:57.880 --> 00:30:02.640
transdermal patch for version of celegentaline that's
used for depression. But in general,

429
00:30:02.680 --> 00:30:04.319
if you see this med on an
exam question, it's usually going to be

430
00:30:04.519 --> 00:30:08.920
referred for its use in Parkinson's disease, so i'd really focus on that indication

431
00:30:10.079 --> 00:30:11.880
rather than for depression. All right, Next, let's talk about the indications

432
00:30:11.880 --> 00:30:15.839
for MAOIs. Is there really anything
we're still using these meds for? So

433
00:30:15.880 --> 00:30:18.799
the short answer is no. For
the exam and for real life, you're

434
00:30:18.839 --> 00:30:23.160
really not going to pick an maoi. These meds will only be used when

435
00:30:23.160 --> 00:30:26.839
all else has failed. And just
like in TCA's it's not that these meds

436
00:30:26.839 --> 00:30:30.720
don't work. They actually work very
well. They just have too damn many

437
00:30:30.799 --> 00:30:34.880
dangerous side effects. So I wouldn't
really bother memorizing indications for these meds as

438
00:30:34.920 --> 00:30:38.559
it's unlikely to be tested on.
So we'll just really briefly run through the

439
00:30:38.559 --> 00:30:41.960
indications. But again I wouldn't memorize
these as it's not usually where you're going

440
00:30:42.000 --> 00:30:45.920
to get tested on so depression.
It's not first line unit to polar depression.

441
00:30:47.000 --> 00:30:49.839
You can use an maoi, but
only when the patient is unresponsive to

442
00:30:51.119 --> 00:30:56.039
several other pharmacotherapy regimens different SSRIs as, centriize, et cetera. This is

443
00:30:56.079 --> 00:31:00.480
not going to be first line.
Other indications refractory cases of panic disorder,

444
00:31:00.559 --> 00:31:04.039
social anxiety disorder, bulimia. Key
here with all of these conditions is again

445
00:31:04.400 --> 00:31:10.519
that MAOIs are not first line meds
only for refractory cases. So probably best

446
00:31:10.559 --> 00:31:14.400
to just mentally skip the indications for
MAOIs, leaving some space in your brain

447
00:31:14.440 --> 00:31:18.480
for something more important, such as
the highest yield thing to know about moois

448
00:31:18.759 --> 00:31:22.039
and what you'll likely get tested on, and that's their adverse effects, So

449
00:31:22.119 --> 00:31:25.920
let's talk about that next. So, MAOIs can cause blurred vision, constipation,

450
00:31:26.079 --> 00:31:30.160
dry mouth, headache, liver enzyme
elevation, orthostatic hypotension, insomnia,

451
00:31:30.240 --> 00:31:32.960
sexual dysfunction. But that's not what
they're going to ask you about. They're

452
00:31:33.000 --> 00:31:36.680
going to ask you about the drug
to drug interactions that can cause serotonin syndrome

453
00:31:36.839 --> 00:31:40.599
and the drug to food interactions that
can cause a hypertensive crisis. That's the

454
00:31:40.680 --> 00:31:42.599
juicy stuff you need to know for
exams. So let's start with probably the

455
00:31:42.640 --> 00:31:45.920
most important of all, and that
is a hypertensive crisis. So if you

456
00:31:45.960 --> 00:31:49.680
take an maoi and eat some cheese, you can have a hypertensive crisis and

457
00:31:49.759 --> 00:31:53.200
potentially die. Hopefully, it's starting
to become a bit more clear why we

458
00:31:53.240 --> 00:31:56.559
don't use these meds so much anymore. So let's elaborate on this a bit.

459
00:31:56.640 --> 00:32:00.039
So. Monominoxidase, as we discussed
before, it's not just found in

460
00:32:00.039 --> 00:32:02.599
the brain, it's found all over
the body, including the lining of the

461
00:32:02.599 --> 00:32:07.519
gut wall, and one of its
jobs in the GI tract, mainly MOOA

462
00:32:07.960 --> 00:32:10.920
is to break down something called tiramine. But in a patient taking in maoi,

463
00:32:12.200 --> 00:32:15.319
as we know, this drug inhibits
monomine oxidase, meaning tiamine isn't broken

464
00:32:15.359 --> 00:32:19.480
down as it should be. So
out of this matter well, tiramine in

465
00:32:19.559 --> 00:32:24.240
high concentrations can increase nor epinephrine release. Nor epic can cause vasoconstriction, increased

466
00:32:24.240 --> 00:32:28.599
heart rate, and cause a rise
in blood pressure, which can precipitate a

467
00:32:28.680 --> 00:32:31.799
hypertensive crisis. Long story short,
MOOI is combined with foods that have a

468
00:32:31.799 --> 00:32:36.319
bunch of tiramine can cause your BP
to go sky high, so you want

469
00:32:36.359 --> 00:32:38.200
to avoid that. Now, what
foods have a lot of tiamine in them?

470
00:32:38.400 --> 00:32:42.359
The main ones are cheese, meat, poultry, fish, beer,

471
00:32:42.640 --> 00:32:45.400
and really any aged or fermented food. If you're a gain of thronespan,

472
00:32:45.480 --> 00:32:49.319
I have a way for you to
remember which foods are high in tiamine.

473
00:32:49.519 --> 00:32:53.480
So tiamine sounds a lot like Tyrian
Lanister and Tiian he liked his tiamine rich

474
00:32:53.559 --> 00:32:59.240
foods, beer and other alcohol as
well as those classic medieval foods cheese,

475
00:32:59.279 --> 00:33:01.640
meats for men or spoiled food.
So if you can't remember which foods are

476
00:33:01.720 --> 00:33:05.960
high in tiamine, just think what
did Tyian Lanister eat and drink back in

477
00:33:06.000 --> 00:33:08.160
those medieval times? And that's your
answer. At least that's how I remembered

478
00:33:08.160 --> 00:33:10.319
it, all right. Last thing, you need to know these meds can

479
00:33:10.359 --> 00:33:14.799
cause serotonin syndrome. So yes,
all of the meds we went over today

480
00:33:14.839 --> 00:33:19.519
can potentially cause serotonin syndrome. So
this isn't unique to MAOIs. But what

481
00:33:19.680 --> 00:33:22.559
is unique to MAOIs and why it's
often tested on, is that episodes of

482
00:33:22.599 --> 00:33:29.480
serotonin syndrome involving in Maoi versus other
classes are generally more severe and can potentially

483
00:33:29.559 --> 00:33:31.319
be fatal, so you really want
to be careful with this class of medication.

484
00:33:31.440 --> 00:33:36.480
You never want to mix an MAOI
with another serotonergic agent like an SSRI,

485
00:33:36.680 --> 00:33:38.519
s centrii, et cetera. So
that's really important. And there are

486
00:33:38.599 --> 00:33:42.960
of course a lot of side effects
for MAOIs, but make sure you really

487
00:33:42.960 --> 00:33:46.759
focus on your hypertensive crisis with tiramine
rich foods and serotonin syndrome, that's likely

488
00:33:46.799 --> 00:33:50.279
what will be tested on. Okay, so we're almost to the end here.

489
00:33:50.319 --> 00:33:52.400
There's three other antidepressants I want to
go over that don't fall into any

490
00:33:52.440 --> 00:33:55.519
of the above classes, but they
come up very frequently on exams, so

491
00:33:55.640 --> 00:34:00.359
let's briefly go over them. So
first one is bupropion. This is a

492
00:34:00.400 --> 00:34:06.039
really high yield meant to know.
Bupropeon is considered an atypical antidepressant atypical as

493
00:34:06.119 --> 00:34:08.800
the way it works is distinct from
the other classes we have gone over thus

494
00:34:08.840 --> 00:34:13.320
far, a SSRIs, at centarize, etc. What you'll find with these

495
00:34:13.320 --> 00:34:17.360
atypicals is they have some unique characteristics
which can make them desirable for certain patient

496
00:34:17.360 --> 00:34:20.960
populations. You'll see what I mean
in a minute. So how does this

497
00:34:21.039 --> 00:34:25.400
medication work. How's it different?
Well, bupropeon inhibits presynaptic reuptake of dopamine

498
00:34:25.400 --> 00:34:30.079
and nor epinephrine, which leads to
increased levels of these neurotransmitters within the synaptic

499
00:34:30.159 --> 00:34:34.440
left. Now, how is this
different than the other antidepressants we've gone over

500
00:34:34.519 --> 00:34:37.840
so far. The main difference you'll
notice is bupropion has little to no effect

501
00:34:37.920 --> 00:34:42.599
on serotonin. Unlike all of the
other classes we have gone over so far,

502
00:34:43.079 --> 00:34:45.360
SSRIs, as, centraized, TCA's, etc. Which did have an

503
00:34:45.360 --> 00:34:50.480
impact on serotonin, bupropion does not, and its main effect is only on

504
00:34:50.519 --> 00:34:52.920
dopamine and nor epi. All Right, so there's a few other high yield

505
00:34:52.960 --> 00:34:57.840
things you need to know for bupropion, and I recommend committing these to memory

506
00:34:57.880 --> 00:35:00.360
because they really like to make exam
questions on this. So luckily, everything

507
00:35:00.400 --> 00:35:05.440
you need to know about bupropion starts
with the letter S at least it does

508
00:35:05.480 --> 00:35:08.400
formynomonics. So here's the four s's
you need to know for this medication,

509
00:35:08.599 --> 00:35:13.599
which are seizures, smoking, skinny, and sex. You're very likely going

510
00:35:13.599 --> 00:35:15.760
to get a question on one of
those, so let's break them down,

511
00:35:15.880 --> 00:35:20.000
starting with the first S that stands
for seizures, So this is a very

512
00:35:20.000 --> 00:35:23.800
important thing to know. Bupropion can
cause generalized seizures. The higher the dose,

513
00:35:23.920 --> 00:35:28.000
the higher the risk of a seizure. So you want to avoid using

514
00:35:28.000 --> 00:35:31.719
these in patients at risk for seizures, so patients withdrawing from alcohol, benzos,

515
00:35:31.800 --> 00:35:36.880
barbituates, et cetera. And then
the highest deeled patient populations that's at

516
00:35:36.960 --> 00:35:38.440
risk for seizures. At least for
the sake of an exam, the one

517
00:35:38.440 --> 00:35:43.000
that's always tested on is a patient
with the history of eating disorders, so

518
00:35:43.079 --> 00:35:45.800
anorexia, bulimia. They always ask
questions on this. You need to know

519
00:35:46.119 --> 00:35:51.280
you do not use bupropion in a
patient that has a high risk for seizures,

520
00:35:51.519 --> 00:35:53.719
especially those patients with eating disorders.
You can thank me later when you

521
00:35:53.760 --> 00:35:57.880
get this question right on your exam
because they always ask it. Next S

522
00:35:57.880 --> 00:36:01.360
stands for sex, So bupropion is
the antidepressant of choice if you want to

523
00:36:01.400 --> 00:36:06.079
avoid sexual side effects. So if
you have a patient who's concerned about sexual

524
00:36:06.159 --> 00:36:08.599
side effects, is going to start
an antidepressant, or maybe a patient who's

525
00:36:08.599 --> 00:36:14.119
already experiencing sexual side effects from SSRIs, which we know can cause that switch

526
00:36:14.159 --> 00:36:17.840
them to bupropion. There's even some
studies that show benefit from adding bupropeon to

527
00:36:17.960 --> 00:36:22.039
an SSRI to help mitigate the sexual
side effects experience, so you definitely need

528
00:36:22.079 --> 00:36:25.119
to know this. It'll likely be
tested on. I used to remember if

529
00:36:25.199 --> 00:36:30.480
you add an M to bupropeon after
the U, it made bump ropeon bump

530
00:36:30.599 --> 00:36:36.039
ropeon bump because it's the antidepressant of
choice if you want to bump in grind,

531
00:36:36.239 --> 00:36:39.639
so remember it as bump ropeon instead
of bupropeon to remember antidepressant of choice

532
00:36:39.679 --> 00:36:44.159
if you want to bump and grind. Next S is smoking pretty straightforward.

533
00:36:44.320 --> 00:36:47.719
Bupropeon is one of the first line
pharmacotherapies that can be used to assist with

534
00:36:47.800 --> 00:36:52.559
smoking cessation. So another important S
for smoking and then the last S stands

535
00:36:52.599 --> 00:36:58.159
for skinny. So bupropion, unlike
some other classes, does not generally cause

536
00:36:58.199 --> 00:37:00.400
weight gain. In fact, a
metal noalo is found that on average,

537
00:37:00.440 --> 00:37:06.000
patients taking bupropion actually lost around one
kilogram. So if you have a patient

538
00:37:06.000 --> 00:37:08.440
who's fear full of weight game with
the other classes, this is another compelling

539
00:37:08.480 --> 00:37:13.199
reason to use bupropion as it can
cause weight loss. They actually have a

540
00:37:13.199 --> 00:37:17.280
weight loss medication called contrave which is
just a combination of bupropion and nowtrexone.

541
00:37:17.480 --> 00:37:21.920
So if you remember those four s's
four bupropion, very likely you'll get the

542
00:37:22.000 --> 00:37:25.320
question right again, seizure, sex, smoking, and skinny. Next atypical

543
00:37:25.360 --> 00:37:29.119
to know is mere tazepine. There's
not a lot to know for this one.

544
00:37:29.239 --> 00:37:31.239
One major point will go over in
a second. So the mechanism of

545
00:37:31.400 --> 00:37:35.800
action for meretazipine, it's kind of
complex. There's a lot going on.

546
00:37:36.000 --> 00:37:37.360
I don't think you need to know
all of the specifics, but the main

547
00:37:37.400 --> 00:37:43.920
thing to know is that this drug
antagonizes presynaptic alpha two adrenergic receptors. That's

548
00:37:43.960 --> 00:37:50.760
really important. Antagonizes pre synaptic alpha
two adreenetic receptors and post synaptics serotonin five

549
00:37:51.000 --> 00:37:53.639
H two and serotonin five HT three
receptors. So I'm going to break this

550
00:37:53.679 --> 00:37:57.079
down, but for the exam again, remember if you can just remember this

551
00:37:57.119 --> 00:38:00.800
drug antagonizes alpha two receptors, probably
be enough to get the question right.

552
00:38:00.840 --> 00:38:02.679
But we'll dive a little deeper for
the sake of understanding. Let's first start

553
00:38:02.719 --> 00:38:07.519
with the alpha two adrenergic receptors.
We didn't really talk about these receptors yet

554
00:38:07.559 --> 00:38:10.519
because most of the antidepressants didn't work
on this specific area. Last, why

555
00:38:10.559 --> 00:38:15.599
this is considered an atypical antidepressant,
But alpha two adrenergic receptors. They're mainly

556
00:38:15.639 --> 00:38:20.920
found in the presynaptic neuron and they
work primarily through a negative feedback loop.

557
00:38:21.159 --> 00:38:23.519
For instance, when nor epi is
released, some of it binds to these

558
00:38:23.519 --> 00:38:28.880
alpha two receptors, which in turn
inhibits further release of neropinephrin. So this

559
00:38:28.960 --> 00:38:31.960
medication blocks these receptors so that negative
feedback loop is shut off, and in

560
00:38:32.000 --> 00:38:37.559
turn we have more nor epinefrin released
as well as serotonin through an additional pathway,

561
00:38:37.119 --> 00:38:42.559
so that's good. In addition,
this medication also has an antagonistic effect

562
00:38:42.599 --> 00:38:47.760
on postsynaptic serotonin five HT two and
serotonin five HT three receptors, so it

563
00:38:47.800 --> 00:38:55.239
basically blocks certain serotonin receptors, which
sounds counterintuitive blocking serotonin receptors, but by

564
00:38:55.280 --> 00:39:00.400
blocking these two specific receptors, redirecting
it away from five HT two and five

565
00:39:00.599 --> 00:39:05.480
HG three, this allows them to
bind to a more useful receptor known as

566
00:39:05.519 --> 00:39:08.519
the five HT one a receptor,
which has a stronger effect on depression.

567
00:39:08.599 --> 00:39:14.119
This medication also has a high affinity
for histamine H one receptors, which accounts

568
00:39:14.119 --> 00:39:16.880
for some of its side effects.
Again, this is a complicated mechanism.

569
00:39:16.960 --> 00:39:21.000
I don't think it's necessary to know
all of this, and you probably won't

570
00:39:21.000 --> 00:39:23.480
even be asked about this on the
exam, but you are likely going to

571
00:39:23.519 --> 00:39:27.519
be asked about in the main and
possibly the only thing you need to know

572
00:39:27.559 --> 00:39:31.159
from mertazipine is that it stimulates appetite
and causes weight gain. This is so

573
00:39:31.519 --> 00:39:35.800
high yield, I definitely got a
question on it. Martazipine has a big

574
00:39:35.800 --> 00:39:39.320
impact on appetite and could cause significant
weightain, up to a seven percent increase

575
00:39:39.360 --> 00:39:43.320
in body weight. This can be
seen in short and long term use.

576
00:39:43.400 --> 00:39:45.199
You need to remember that it's always
asked about, So how are you going

577
00:39:45.239 --> 00:39:49.400
to remember that? Well, instead
of remembering mere tazipine, I want you

578
00:39:49.440 --> 00:39:53.519
to remember it as meal tazipine,
meal meal, meal tazipine. Because you

579
00:39:53.519 --> 00:39:59.159
remember this can stimulate appetite, making
patients finish their meals and gain weight.

580
00:40:00.000 --> 00:40:02.519
They're less important side effect to be
aware of is sedation. Close to twenty

581
00:40:02.519 --> 00:40:07.039
percent of patients will have drowsiness or
sedation, which is likely due to the

582
00:40:07.159 --> 00:40:10.519
drugs high affinity for histamine H one
receptors. But focus on the weight gain

583
00:40:10.559 --> 00:40:14.679
as that's the most important thing to
know, all right. So last ndepressent

584
00:40:14.719 --> 00:40:17.239
we're going to go over as trasidone. So trasidone is in a class of

585
00:40:17.239 --> 00:40:22.360
meds called serotonin modulators. There's a
few other drugs in this class and the

586
00:40:22.440 --> 00:40:25.440
fazodone velazidone, but trazodone is the
one you'll likely get tested on. So

587
00:40:25.559 --> 00:40:32.880
trasidone inhibits presynaptic serotonin reuptake and acts
as an antagonist at the five HT two

588
00:40:32.920 --> 00:40:37.599
A and two C serotonin receptors.
So both of these mechanisms we've gone over

589
00:40:37.639 --> 00:40:44.079
with other medications. So trasidone weekly
inhibits presynaptic serotonin reuptake, so same thing

590
00:40:44.119 --> 00:40:47.239
we saw with SSRIs blocks reuptake up
serotonin, so we have more serotonin hanging

591
00:40:47.239 --> 00:40:51.440
out in the synaptic left to do
its thing. And then this drug also

592
00:40:51.639 --> 00:40:58.480
blocks serotonin receptors, specifically post synaptic
serotonin five HT two A and five HT

593
00:40:58.679 --> 00:41:02.280
two C receptors. So We talked
about this with mertazipine, basically redirecting serotonin

594
00:41:02.360 --> 00:41:07.400
away from certain receptors, causing them
to bind with more useful ones. Now

595
00:41:07.480 --> 00:41:12.519
trazodone, it's a bit sloppy and
it also affects alpha adrenertic receptors and histamine

596
00:41:12.599 --> 00:41:16.519
H one receptors which causes some high
yield. Very often tested on side effects

597
00:41:16.559 --> 00:41:20.320
you need to know for your exam. This is another drug where the side

598
00:41:20.320 --> 00:41:23.119
effects are the most commonly tested on
aspect of the drug. So first one

599
00:41:23.199 --> 00:41:29.039
is sedation. A study found that
sixty one percent of patients taking traszone experience

600
00:41:29.119 --> 00:41:32.360
sedation. This is likely due to
the strong effect this medication has on histamine

601
00:41:32.440 --> 00:41:37.199
H one receptors, so you'll often
see this medication being used off label for

602
00:41:37.280 --> 00:41:39.320
patients with insomnia, so you need
to know this. And the other side

603
00:41:39.320 --> 00:41:43.400
effect you need to know, a
rare but serious one that's often tested on

604
00:41:43.559 --> 00:41:47.400
is priapism. So priapism a persistent
erection. While rare, can happen with

605
00:41:47.400 --> 00:41:52.039
this medication, it's a medical emergency
and while it's not common, they love

606
00:41:52.079 --> 00:41:53.960
to test on it. And it
has to do with the medications effect on

607
00:41:54.000 --> 00:41:58.719
alpha adrenergic receptors. So you definitely
need to know both of these side effects.

608
00:41:58.719 --> 00:42:00.119
They're likely going to be on your
exist and the way that you're going

609
00:42:00.159 --> 00:42:05.039
to remember them is by instead of
remembering trazodone, I want you to instead

610
00:42:05.079 --> 00:42:10.079
remember trasabone traszebone, so tras with
a bunch of dizas to help you remember

611
00:42:10.119 --> 00:42:15.000
the sedation commonly experienced with this medication, and bone to help your remember priapism,

612
00:42:15.079 --> 00:42:17.920
the boner that just won't quit.
So those are the two high old

613
00:42:17.920 --> 00:42:21.760
things you need to know for this
medication, and that's why you'll likely be

614
00:42:21.800 --> 00:42:24.480
tested on. Remember trasabone and you
should be good. All right, So

615
00:42:24.519 --> 00:42:28.559
that was your antidepressants. It's a
lot, but stick to the unique,

616
00:42:28.639 --> 00:42:30.760
high old stuff. Remember the namonics
we went over, and you'll likely be

617
00:42:30.840 --> 00:42:36.079
Okay. Let's do five quick questions
to see what you retained. Question one.

618
00:42:36.440 --> 00:42:39.599
A sixty seven year old male presents
the office today complaining of persistent low

619
00:42:39.679 --> 00:42:45.119
mood and hedonia and feelings of hopelessness
that have been affecting his daily life for

620
00:42:45.159 --> 00:42:49.159
the past several months. Additionally,
he reports tingling and burning pain in both

621
00:42:49.199 --> 00:42:52.800
of his feet over the past few
years. And is seeking medication to alleviate.

622
00:42:52.840 --> 00:42:57.280
This patient has a history of type
two diabetes, hyperlipidemia, and diabetic

623
00:42:57.320 --> 00:43:01.679
neuropathy. His current medications include glomepera
and resove a statin. Patient was diagnosed

624
00:43:01.719 --> 00:43:07.119
with depression and the decision is made
to initiate pharmacotherapy. Which of the following

625
00:43:07.239 --> 00:43:13.599
choices would be most appropriate for the
patient mentioned above A meritazepine, B bupropion,

626
00:43:14.079 --> 00:43:22.800
C duloxetine, D S catalopram or
E fluvoxamine. So that is going

627
00:43:22.840 --> 00:43:28.119
to be C duloxetine. So we
have a bunch of different medications that could

628
00:43:28.159 --> 00:43:31.679
all potentially treat this patient's depression.
But the question also mentions this patient has

629
00:43:31.840 --> 00:43:37.880
untreated diabetic neuropathy evident by the tingling
and burning pain in his feet, in

630
00:43:37.920 --> 00:43:40.679
which he is also seeking treatment,
And there's only one medication listed here that

631
00:43:40.719 --> 00:43:45.920
can treat both his depression and neuropathic
pain, and that's duloxetine. Duloxetine,

632
00:43:45.960 --> 00:43:50.599
as we know, is an SNRI. It's often preferred in patients with comorbid

633
00:43:50.639 --> 00:43:54.480
depression and chronic pain conditions such as
diabetic neuropathy. So remember, instead of

634
00:43:54.559 --> 00:44:00.920
duloxetine. Remember dual oxetine for the
dual indication for both depression and chronic pain

635
00:44:00.280 --> 00:44:05.280
making and an appropriate choice in this
patient. Question two, the decision is

636
00:44:05.280 --> 00:44:08.719
made to initiate antidepressant therapy and a
twenty eight year old female with a recent

637
00:44:08.760 --> 00:44:15.480
diagnosis of major depressive disorder. Past
medical history includes hypertension, hyperlipidemia, and

638
00:44:15.559 --> 00:44:20.599
coeliac disease. She states her friend
found great success with cytalopram and was wondering

639
00:44:20.639 --> 00:44:23.480
if she could try this medication.
Upon reviewing her past medical records, you

640
00:44:23.519 --> 00:44:29.119
find a family history of unexplained syncope
and sudden cardiac arrest. What should be

641
00:44:29.199 --> 00:44:36.920
ruled out before starting this patient on
citalopram. So that is going to be

642
00:44:37.000 --> 00:44:40.840
QT prolongation. So ctalopram is an
SSRI and one of the biggest concerns with

643
00:44:40.880 --> 00:44:45.159
this medication is QT prolongation. You
want to avoid this medication in patients with

644
00:44:45.239 --> 00:44:51.039
congenital long QT syndrome or any other
risk factors for prolonged QT syndrome. So

645
00:44:51.079 --> 00:44:53.960
you have a patient with the family
history of unexplained syncope sudden cardiac arrest.

646
00:44:54.320 --> 00:44:59.440
Patient definitely needs a work up to
ensure she doesn't have congenital long QT syndrome

647
00:44:59.599 --> 00:45:04.199
given her family history. Remember the
main ssrise where QT prolongation is a concern

648
00:45:04.440 --> 00:45:08.199
cetalopram first and foremost and esctalopram.
And if you remember the sentence, if

649
00:45:08.239 --> 00:45:12.280
you long for quiet time, you
need to escape the city, You'll never

650
00:45:12.320 --> 00:45:15.599
forget the SSRIs that carry the risk
for QT prolongation. Long for quiet time,

651
00:45:15.679 --> 00:45:21.880
long QT escape esketealopram city, cetalopram. Question three. A thirty two

652
00:45:21.960 --> 00:45:23.960
year old male with the history of
depression has been treated with searchulene for the

653
00:45:23.960 --> 00:45:29.559
past six months. He initially showed
improvement in his mood, but developed bothersome

654
00:45:29.719 --> 00:45:35.280
sexual side effects, including decreased libido
and difficulty achieving and maintaining erection. In

655
00:45:35.320 --> 00:45:37.559
response to these side effects, you
decide to decrease the SSR I dose,

656
00:45:37.800 --> 00:45:43.639
but the sexual side effects persist.
Which medication would be most appropriate to replace

657
00:45:43.679 --> 00:45:51.760
cetralene in this patient A citalopram,
B bupropion, C fluoxetine, D peroxetine

658
00:45:51.880 --> 00:46:00.840
or e venlefaccine, So that's B
bupropion, so bupropion and atypical antidepressant.

659
00:46:00.880 --> 00:46:04.280
As we discussed before, does not
have the sexual side effects that we see

660
00:46:04.320 --> 00:46:08.719
in ssrise and is very commonly the
antidepressant of choice for a patient experiencing sexual

661
00:46:08.760 --> 00:46:15.000
side effects. So remember bump ropeon
instead of bupropeon, as it's the antidepressant

662
00:46:15.000 --> 00:46:17.280
of choice if you want to bump
and grind. All the other choices are

663
00:46:17.320 --> 00:46:22.800
either ssrise or snrise, which all
carry the risk of sexual side effects.

664
00:46:22.000 --> 00:46:25.079
Question four. A fifty eight year
old male is spending a night out with

665
00:46:25.159 --> 00:46:30.400
friends celebrating a recent promotion. He
is enjoying a few beers as well as

666
00:46:30.400 --> 00:46:35.840
some appetizers of age cheese cured meats
when he begins to experience headache, nausea,

667
00:46:35.880 --> 00:46:38.440
and chest pain. Paramedics were called
to the scene and his blood pressure

668
00:46:38.480 --> 00:46:42.960
is reported to be one eight four
over one twenty two. He reports he

669
00:46:43.039 --> 00:46:46.320
was recently started on a new medication
for his refractory depression, but does not

670
00:46:46.360 --> 00:46:52.000
recall the name. Which of the
following antidepressants is He most likely taking a

671
00:46:52.360 --> 00:47:00.719
certralene, B mertazepine, C fluvoxamine, D phenylzene or E S catalopram,

672
00:47:00.800 --> 00:47:05.039
So that is going to be D
fenelzine, So we know this is a

673
00:47:05.119 --> 00:47:07.960
hypertensive crisis. We know this was
caused by an maoi due to the high

674
00:47:07.960 --> 00:47:12.639
amounts of tiramine he consumed, beer, cheese, etc. So all we

675
00:47:12.679 --> 00:47:15.559
have to figure out at this point
is which one of these is an maoi.

676
00:47:15.639 --> 00:47:17.159
So even if you can't remember the
names of all of the MAOIs,

677
00:47:17.199 --> 00:47:21.760
which I don't blame you. If
you can at least remember the mnemonics tips,

678
00:47:21.800 --> 00:47:24.400
tips, you can narrow it down
so we know all of the MAOIs

679
00:47:24.440 --> 00:47:29.159
at least here in the US.
Start with the letters tips, so that

680
00:47:29.239 --> 00:47:31.079
narrows it down to just two meds
in these answers. So you have a

681
00:47:31.079 --> 00:47:35.519
fifty percent chance of getting it righteous
by using this mnemonic And if you can

682
00:47:35.559 --> 00:47:39.000
remember that Serchralene is an SSRI from
the Serpent Snake Charmer pneumonic, you know

683
00:47:39.119 --> 00:47:44.480
all that's left is fenolzine and maoi
And that's the correct answer for this question.

684
00:47:44.800 --> 00:47:47.400
Final question number five. A thirty
eight year old female presents to the

685
00:47:47.400 --> 00:47:52.239
office to follow up on her recent
diagnosis of depression. At the last visit,

686
00:47:52.280 --> 00:47:54.559
the decision was made to start psychotherapy, but she finds this to be

687
00:47:54.599 --> 00:47:59.679
ineffective and is seeking medication to improve
her mood. She's not currently taking any

688
00:47:59.679 --> 00:48:04.679
personscryption medication, denies a family history
of depression, and has no other medical

689
00:48:04.679 --> 00:48:07.559
conditions. This will be her first
time taking an antidepressant, and her only

690
00:48:07.639 --> 00:48:12.119
concern is the potential for weight gain, as she has struggled with her weight

691
00:48:12.159 --> 00:48:15.320
in the past. Which medication listed
below would be most appropriate to start in

692
00:48:15.360 --> 00:48:23.760
this patient A isocarboxyzid, B doxipin, c amatryptylene, D fluoxetine, or

693
00:48:23.840 --> 00:48:30.960
E peroxetine, So that's going to
be D fluoxetine. So we have a

694
00:48:31.000 --> 00:48:36.960
patient with no medical conditions who's going
to start pharmacotherapy for depression. She hasn't

695
00:48:36.960 --> 00:48:39.119
tried any mets. We know we
start with our first line medications, and

696
00:48:39.159 --> 00:48:44.360
we know TCAs and MAOIs are never
first line treatments for depression. So right

697
00:48:44.400 --> 00:48:47.320
off the bat, you can eliminate
isocarboxyxid and maoi, and you can eliminate

698
00:48:47.400 --> 00:48:52.960
doxipin and amatriptlene, which are TCAs. So what we're left with is fluoxetine

699
00:48:52.000 --> 00:48:57.159
and peroxetine. Both of these are
SSRIs. So which one is the right

700
00:48:57.199 --> 00:49:00.360
answer? Well, technically, either
one of these would be a probe to

701
00:49:00.400 --> 00:49:05.599
treat her depression. But she mentioned
she's concerned about wekain and we know peroxetine

702
00:49:05.639 --> 00:49:08.760
is the SSRI associated with the most
weight gain, remember our fat parrot,

703
00:49:09.000 --> 00:49:13.880
And since this is a concern of
hers, fluoxetine would be the most appropriate

704
00:49:13.960 --> 00:49:15.760
choice in this patient. All right, So that is your antidepressants. I

705
00:49:15.760 --> 00:49:19.559
hope that was helpful. Thank you
so much for listening, and good luck

706
00:49:19.599 --> 00:49:20.039
in school.

