November 1, 2023 • 11 mins
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In this episode of The Y in Psychiatry, Dr. Amayo and Dr. Handratta explore the potentially potent side effects of SSRIs (selective serotonin reuptake inhibitors). They discuss the risks of switching to mania, the role of mood stabilizers, the increased risk of suicidality in younger patients, and the common side effects of nausea and vomiting. Tune in as they delve into the intricacies of psychiatric medication and its impact on the human experience.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Thanh (00:01):
Welcome to the Y in Psychiatry!
Dr. Amayo (00:03):
Hi, this is Dr.
Amayo C/L fellow.
Thanh (00:06):
Where we delve into the intricate nuances of psychiatric
topics.
Dr. Handratta (00:09):
My name is Dr.
Handratta attendingpsychiatrist.
I did my residency fromUniversity of Connecticut and
then I did my fellowship fromGeorgetown University in
consultation and liaison.
Thanh (00:19):
Each episode features interview style discussions that
explore the intersection of themind medicine and the human
experience.
Together we'll uncover thehidden why and the
groundbreaking discovery shapingthe psychiatric landscape.
So grab a seat, warm beverage,tune in, and let's embark on
this journey to unlock themysteries of the human psyche.
(00:43):
Only on The Y in Psychiatry.
Dr. Amayo (00:46):
Welcome to the Y in psychiatry.
Today we will be talking aboutwhy we get the side effects from
SSRIs.
As usual, it's your host, Dr.
Amayo, and I am here with Dr.
Handratta
Dr. Handratta (01:01):
Hello guys.
How are you guys doing?
Dr. Amayo (01:03):
I've found myself explaining to patients the side
effects and one of the bigthings that I tell them is,
they're gonna have some GIsymptoms, some nausea.
Then another thing I, I askthem, I tell them is, the risk
of switching to mania.
So that's a big warning.
And another big black boxwarning is the increase in
suicidality.
So, Sir, I was wondering if wecan start with why does SSRI
(01:25):
increases your chance of mania?
how does that work?
Dr. Handratta (01:28):
How does antidepressants actually switch
a person into manic episode?
So whenever we prescribeantidepressants, we always want
to make sure, or whenever weevaluate any psychiatric patient
we basically need to make surethat we rule out bipolar
disorder.
The best way to rule out bipolardisorder is by using scales like
mood disorder questionnaire.
Or rapid mood screening, whichwill screen a patient.
(01:50):
If they are positive, then thatmeans that there's a high
probability that the patientmight have bipolar disorder.
Then you have to actually go fora detailed history taking.
So you guys know exactly whereI'm heading towards.
So if a patient has bipolardisorder, then we stay away from
conventional antidepressantsbecause we know that they can
switch a patient into mania
Dr. Amayo (02:07):
I have a question.
Does SSRI cause someone to havemanic episode or cause them to
have bipolar, or does it justincreases their, so are they
already like bipolar and SSRIjust increases their chances of
them switching?
Dr. Handratta (02:21):
So SSRIs without a mood stabilizer in a patient
who has bipolar disorder,increases the risk or switch
into a manic or a hypomanicepisode
Dr. Amayo (02:31):
Yes.
And if the patient never hasbipolar disorder or doesn't have
a risk of bipolar disorder,would an SSRI increase that
risk?
I guess that was, that's myquestion.
Dr. Handratta (02:40):
No, it will not.
Dr. Amayo (02:40):
So if the baseline are not likely to have bipolar
disorder, the SSRI would not.
Dr. Handratta (02:45):
No.
Okay.
It will not increase the patientdoesn't have bipolar disorder at
all and doesn't have any familyhistory of bipolar disorder.
Okay.
Now, You have to be a littlecareful when you introduce an
SSRI because patients can haveside effects like increased
agitation Irritability andrestlessness for the first one
to two weeks.
That is, especially because ofserotonin hypersensitivity it
(03:05):
does not mean that the patientis switching But I think the
screening will be extremelyhelpful because if you look at
the bipolar data, about 70% ofthe patients are actually not
diagnosed when they come duringthe initial visit 35% of the
patients with bipolar will notbe diagnosed for 10 years And
they would've gone throughalmost three and a half
diagnosis or through fourdifferent physicians before they
(03:26):
get diagnosed with bipolar.
So you need to be careful.
And in the primary care clinic,out of every five patients that
they diagnosed with thedepression there'll be one
patient who will have bipolardisorder.
So always a good idea to screenthe patient.
Now what are the risks?
We see in our practice that alot of providers will use
conventional antidepressantswith mood stabilizer.
(03:47):
So what's the data availableWhen you use a mood stabilizer
and use SSRI with a moodstabilizer, the risk of switch
is less than placebo.
Dr. Amayo (03:55):
And this is for patients that already have
confirmed bipolar disorder?
Dr. Handratta (03:58):
Exactly.
So and the, the, basically thereason when you use SSRI for a
long period of time, itdecreases the sensitivity of the
beta adrenergic receptors.
So under stressful situation,when the norepinephrine level
goes up, you do not have thebeta adrenergic receptors to
attach to.
So that is one of the theorybehind why SSRIs is when used
with mood stabilizer risk ofswitching to mania is equivalent
to placebo.
Dr. Amayo (04:19):
That's the SSRIs, yes.
Yes.
But it doesn't do that when it'sgiven alone.
Dr. Handratta (04:23):
So when it's given alone, you don't have a
mood stabilizer on board.
If you don't have a moodstabilizer on board, then the
risk actually increases.
But I would advise with a moodstabilizer try to use an FDA
recommended medication forbipolar depression rather than
conventional antidepressant.
Unless they've failedeverything.
Now, what's the data on moodstabilizers with Bupropion?
The data actually shows thatwhen you use mood stabilizer
(04:44):
with bupropion for bipolardepression, the risk of switch
is less than placebo.
One of the hypothesis is thatBupropion is not a very potent
norepinephrine and dopaminereuptake inhibitor.
Plus, it does not act on thepostsynaptic receptors like
other antidepressants.
The risk actually with a moodstabilizer plus an SNRI like or
with the TCA tricyclicantidepressant, the risk of
switching is more than placebo.
(05:05):
So I would advise, don't eventouch SNRI or TCA with a mood
stabilizing bipolar patient.
Dr. Amayo (05:10):
Is there a reason?
Do we have any theories as towhy?
Dr. Handratta (05:13):
So there are, so again, everything is in
hypothesis.
We do not know for sure.
There's a lot of research datafloating around.
But one of the most possibleexplanation is that when you use
tricyclic antidepressant is thatit is the anticholinergic effect
that causes the switch to mania.
That ability to block the M2 andM4 muscarinic receptor.
As well as a N-acetylcholinereceptor.
That switches them into a manicepisode.
(05:34):
With an SNRI, when you use SNRIat a higher dose, they also
increase the dopamine.
Oh, For example, venlafaxine.
When you use 225 and above, itactually will hit the dopamine,
and with des venlafaxine, whenyou go actually close to a
hundred or more, it willincrease the dopamine.
Dr. Amayo (05:48):
So sir, I guess the next question would be, So just
without the mood stabilizer.
Why does antidepressantsincreases the risk of switching
to mania?
Dr. Handratta (05:59):
So now we heard about like why we don't use
conventional antidepressantswith the mood stabilizer.
So the research data that youactually see says that when you
use conventional antidepressant,there are different reasons why
your patient switches intomania.
One reason actually is that whenyou use antidepressant over a
long period of time, it causesdecreased sensitivity of the
(06:21):
pre-synaptic dopamine D2receptors.
And we know that pre-synaptic D2receptors are auto receptors,
okay?
So when you decrease thesensitivity of the auto
receptor, you increase therelease of dopamine from the
presynaptic.
The second is it also increasesthe sensitivity of the
postsynaptic dopamine receptor,especially the D2 receptor.
So it's acting in both.
So it's first is increasing theD two and second is making the
(06:44):
postsynaptic receptor moresensitive to the D two.
Which increases your risk of amanic episode.
The next theory is as we talkedabout, the anticholinergic
effects of tricyclicantidepressants.
Dr. Amayo (06:53):
And so sir to, to summarize so why there's an
increased risk of switchingdominion in just regular normal,
everyday anti-depressant isthere's an reduced sensitivity
in the auto receptors.
And that leads to an increase indopamine from the presynaptic
neuro, and there's double whammywith an increased sensitivity in
the postsynaptic neuron to D tworeceptors.
(07:15):
And so that we increase ourchances of Of switching to mania
and also, again, possibly theanticholinergic effect, which we
see more with the TCAs andpossibly paroxetine which has a
anticholinergic effect.
So I guess next question is thesuicidality.
Why, and especially again, it'sbeen an increased risk in the
younger population.
Dr. Handratta (07:33):
So this is a good question, right?
So we always deal with this.
So in patients 24 years or less,there's a black box warning on
the use of antidepressants.
One reason is that one of thehypothesis that people actually
say is that, did we miss bipolardisorder?
So the patient is too young tobe diagnosed with bipolar
disorder has a of bipolardisorder has had like short
episodes of depression, multipleepisodes of depression before
(07:55):
the age of 25 years So all Soall these are risk factors for
bipolar, right?
But the patient has neverexhibited a manic or hypomanic
symptom.
If uou introduce an SSRI or anantidepressant, did you switch
the patient into a mixed state?
Because the risk of suicide ishigher in patients with bipolar
mixed state.
Now, there is no solid data,which shows that this is the
(08:16):
reason why there's an increasedrisk of suicide, right?
There's a different hypothesis.
So in 2004, I think, so the FDAactually put the black box
warning they updated in 2007saying that depression itself
can actually increase the riskof suicide But I think like the
good, the best practice isactually to educate the patient
24 years or younger about therisk of switching to mania.
(08:37):
And also to educate the familymembers, because when patients
become manic, they have noinsight.
So it's always a good idea toinvolve the family member.
Talk to them about the risk sothat if the patient misses it,
at least the family members canpick it up.
Dr. Amayo (08:49):
That's a good point with it being that younger of
age, maybe there's more of abipolar components to it, and
that would make sense as to whyit's specific for that age group
that, that we see that risk asopposed to older.
But then I wonder if, becausewomen tend to develop, manic
disorder later in life or whatare, if they're risk for
(09:10):
suicidality, Is a little bitmore extended than males.
I don't know.
Dr. Handratta (09:14):
We don't know that exactly.
Because another hypothesis isthat the patient who is
depressed and is suicidal tobegin with, and as the
depression gets better, thereare more energy actually now to
actually complete this.
So there are differenthypothesis, but none of these
hypothesis has been proven.
Dr. Amayo (09:26):
Yeah, sir.
And then lastly Why do nauseaand vomiting?
I think that's the most commonside effects with our regular
antidepressants.
How about that?
Dr. Handratta (09:36):
So why do we develop nausea?
So the, so there are differenttypes of serotonin receptors
right?
So there's one group ofserotonin receptor called five
HT three receptors, five HTthree, which is basically an
ionotropic receptors It's not aG-protein couple receptor.
So these five HT three receptorsare located in your gut.
As well as it's present in theblood-brain barrier.
So when you stimulate them, itusually stimulates nausea,
(09:58):
vomiting, and headaches.
That's the same reason when youare actually using
chemotherapeutic agent forcancer.
What the chemotherapeutic agentdoes is that it usually
stimulates the antichromaffincells in the duodenum to produce
a huge amount of serotonin Whichserotonin.
Which will stimulate the five HTthree receptor causing nausea in
patients receiving chemotherapy.
Oh, and that's why you have fiveHT three antagonists like
ondansetron So these areactually used for nausea because
(10:18):
they block the five HT threereceptors.
Dr. Amayo (10:21):
And because of their inotropic.
Is that why they work so fast asopposed to the, the typical two
to three weeks before we see thedesired effects we want from
antidepressants.
Dr. Handratta (10:30):
Exactly.
Ionotropic receptors are fasteracting because they are iron
controlled receptors rather thanG protein, which basically uses
a second messenger system.
Dr. Amayo (10:39):
And then I always comfort my patients telling them
that that, the nausea andvomiting will get better after
five to six days.
So do, does this ionotropic fiveHT three receptors get
desensitized to it?
Dr. Handratta (10:52):
So the theory behind actually, when you use
antidepressant for a long periodof time They'll desensitize
these five HT three receptors.
That's when nausea and vomitingdisappears.
After about a week or two weeks?
Sometimes, actually, if it'sreally bad, I sometimes actually
add a five H three antagonist tothe antidepressants so they can
tolerate it better, and aftertwo weeks I slowly take them off
it.
But just make sure that whenyou're giving an antiemetic
(11:13):
agent always makes sure toeducate the patient about
dystonia Especially of the jaw,actually, patient can tell a
dystonic reaction, so it's agood idea to actually educate
them.
But they do develop tolerance toit.
Dr. Amayo (11:24):
Dystonia.
I wasn't tracking that.
Let's talk about it on the nextepisode.
Okay.
Thank you guys and we'll see younext time.
Katrina (11:35):
Thank you for joining us on today's episode.
our tireless team is alreadyhard at work, cobbling together
another potpourri of fascinatingdiscussion for next week, so be
sure to tune in, visit ourwebsite and our podcast feed and
let us know your thoughts on theepisode.
Subscribe so you don't miss ourreleases every Wednesday.
Until next time, keep smiling,keep shining, and stay curious.
Welcome to the Y in Psychiatry!
Dr. Amayo (00:03):
Hi, this is Dr.
Amayo C/L fellow.
Thanh (00:06):
Where we delve into the intricate nuances of psychiatric
topics.
Dr. Handratta (00:09):
My name is Dr.
Handratta attendingpsychiatrist.
I did my residency fromUniversity of Connecticut and
then I did my fellowship fromGeorgetown University in
consultation and liaison.
Thanh (00:19):
Each episode features interview style discussions that
explore the intersection of themind medicine and the human
experience.
Together we'll uncover thehidden why and the
groundbreaking discovery shapingthe psychiatric landscape.
So grab a seat, warm beverage,tune in, and let's embark on
this journey to unlock themysteries of the human psyche.
(00:43):
Only on The Y in Psychiatry.
Dr. Amayo (00:46):
Welcome to the Y in psychiatry.
Today we will be talking aboutwhy we get the side effects from
SSRIs.
As usual, it's your host, Dr.
Amayo, and I am here with Dr.
Handratta
Dr. Handratta (01:01):
Hello guys.
How are you guys doing?
Dr. Amayo (01:03):
I've found myself explaining to patients the side
effects and one of the bigthings that I tell them is,
they're gonna have some GIsymptoms, some nausea.
Then another thing I, I askthem, I tell them is, the risk
of switching to mania.
So that's a big warning.
And another big black boxwarning is the increase in
suicidality.
So, Sir, I was wondering if wecan start with why does SSRI
(01:25):
increases your chance of mania?
how does that work?
Dr. Handratta (01:28):
How does antidepressants actually switch
a person into manic episode?
So whenever we prescribeantidepressants, we always want
to make sure, or whenever weevaluate any psychiatric patient
we basically need to make surethat we rule out bipolar
disorder.
The best way to rule out bipolardisorder is by using scales like
mood disorder questionnaire.
Or rapid mood screening, whichwill screen a patient.
(01:50):
If they are positive, then thatmeans that there's a high
probability that the patientmight have bipolar disorder.
Then you have to actually go fora detailed history taking.
So you guys know exactly whereI'm heading towards.
So if a patient has bipolardisorder, then we stay away from
conventional antidepressantsbecause we know that they can
switch a patient into mania
Dr. Amayo (02:07):
I have a question.
Does SSRI cause someone to havemanic episode or cause them to
have bipolar, or does it justincreases their, so are they
already like bipolar and SSRIjust increases their chances of
them switching?
Dr. Handratta (02:21):
So SSRIs without a mood stabilizer in a patient
who has bipolar disorder,increases the risk or switch
into a manic or a hypomanicepisode
Dr. Amayo (02:31):
Yes.
And if the patient never hasbipolar disorder or doesn't have
a risk of bipolar disorder,would an SSRI increase that
risk?
I guess that was, that's myquestion.
Dr. Handratta (02:40):
No, it will not.
Dr. Amayo (02:40):
So if the baseline are not likely to have bipolar
disorder, the SSRI would not.
Dr. Handratta (02:45):
No.
Okay.
It will not increase the patientdoesn't have bipolar disorder at
all and doesn't have any familyhistory of bipolar disorder.
Okay.
Now, You have to be a littlecareful when you introduce an
SSRI because patients can haveside effects like increased
agitation Irritability andrestlessness for the first one
to two weeks.
That is, especially because ofserotonin hypersensitivity it
(03:05):
does not mean that the patientis switching But I think the
screening will be extremelyhelpful because if you look at
the bipolar data, about 70% ofthe patients are actually not
diagnosed when they come duringthe initial visit 35% of the
patients with bipolar will notbe diagnosed for 10 years And
they would've gone throughalmost three and a half
diagnosis or through fourdifferent physicians before they
(03:26):
get diagnosed with bipolar.
So you need to be careful.
And in the primary care clinic,out of every five patients that
they diagnosed with thedepression there'll be one
patient who will have bipolardisorder.
So always a good idea to screenthe patient.
Now what are the risks?
We see in our practice that alot of providers will use
conventional antidepressantswith mood stabilizer.
(03:47):
So what's the data availableWhen you use a mood stabilizer
and use SSRI with a moodstabilizer, the risk of switch
is less than placebo.
Dr. Amayo (03:55):
And this is for patients that already have
confirmed bipolar disorder?
Dr. Handratta (03:58):
Exactly.
So and the, the, basically thereason when you use SSRI for a
long period of time, itdecreases the sensitivity of the
beta adrenergic receptors.
So under stressful situation,when the norepinephrine level
goes up, you do not have thebeta adrenergic receptors to
attach to.
So that is one of the theorybehind why SSRIs is when used
with mood stabilizer risk ofswitching to mania is equivalent
to placebo.
Dr. Amayo (04:19):
That's the SSRIs, yes.
Yes.
But it doesn't do that when it'sgiven alone.
Dr. Handratta (04:23):
So when it's given alone, you don't have a
mood stabilizer on board.
If you don't have a moodstabilizer on board, then the
risk actually increases.
But I would advise with a moodstabilizer try to use an FDA
recommended medication forbipolar depression rather than
conventional antidepressant.
Unless they've failedeverything.
Now, what's the data on moodstabilizers with Bupropion?
The data actually shows thatwhen you use mood stabilizer
(04:44):
with bupropion for bipolardepression, the risk of switch
is less than placebo.
One of the hypothesis is thatBupropion is not a very potent
norepinephrine and dopaminereuptake inhibitor.
Plus, it does not act on thepostsynaptic receptors like
other antidepressants.
The risk actually with a moodstabilizer plus an SNRI like or
with the TCA tricyclicantidepressant, the risk of
switching is more than placebo.
(05:05):
So I would advise, don't eventouch SNRI or TCA with a mood
stabilizing bipolar patient.
Dr. Amayo (05:10):
Is there a reason?
Do we have any theories as towhy?
Dr. Handratta (05:13):
So there are, so again, everything is in
hypothesis.
We do not know for sure.
There's a lot of research datafloating around.
But one of the most possibleexplanation is that when you use
tricyclic antidepressant is thatit is the anticholinergic effect
that causes the switch to mania.
That ability to block the M2 andM4 muscarinic receptor.
As well as a N-acetylcholinereceptor.
That switches them into a manicepisode.
(05:34):
With an SNRI, when you use SNRIat a higher dose, they also
increase the dopamine.
Oh, For example, venlafaxine.
When you use 225 and above, itactually will hit the dopamine,
and with des venlafaxine, whenyou go actually close to a
hundred or more, it willincrease the dopamine.
Dr. Amayo (05:48):
So sir, I guess the next question would be, So just
without the mood stabilizer.
Why does antidepressantsincreases the risk of switching
to mania?
Dr. Handratta (05:59):
So now we heard about like why we don't use
conventional antidepressantswith the mood stabilizer.
So the research data that youactually see says that when you
use conventional antidepressant,there are different reasons why
your patient switches intomania.
One reason actually is that whenyou use antidepressant over a
long period of time, it causesdecreased sensitivity of the
(06:21):
pre-synaptic dopamine D2receptors.
And we know that pre-synaptic D2receptors are auto receptors,
okay?
So when you decrease thesensitivity of the auto
receptor, you increase therelease of dopamine from the
presynaptic.
The second is it also increasesthe sensitivity of the
postsynaptic dopamine receptor,especially the D2 receptor.
So it's acting in both.
So it's first is increasing theD two and second is making the
(06:44):
postsynaptic receptor moresensitive to the D two.
Which increases your risk of amanic episode.
The next theory is as we talkedabout, the anticholinergic
effects of tricyclicantidepressants.
Dr. Amayo (06:53):
And so sir to, to summarize so why there's an
increased risk of switchingdominion in just regular normal,
everyday anti-depressant isthere's an reduced sensitivity
in the auto receptors.
And that leads to an increase indopamine from the presynaptic
neuro, and there's double whammywith an increased sensitivity in
the postsynaptic neuron to D tworeceptors.
(07:15):
And so that we increase ourchances of Of switching to mania
and also, again, possibly theanticholinergic effect, which we
see more with the TCAs andpossibly paroxetine which has a
anticholinergic effect.
So I guess next question is thesuicidality.
Why, and especially again, it'sbeen an increased risk in the
younger population.
Dr. Handratta (07:33):
So this is a good question, right?
So we always deal with this.
So in patients 24 years or less,there's a black box warning on
the use of antidepressants.
One reason is that one of thehypothesis that people actually
say is that, did we miss bipolardisorder?
So the patient is too young tobe diagnosed with bipolar
disorder has a of bipolardisorder has had like short
episodes of depression, multipleepisodes of depression before
(07:55):
the age of 25 years So all Soall these are risk factors for
bipolar, right?
But the patient has neverexhibited a manic or hypomanic
symptom.
If uou introduce an SSRI or anantidepressant, did you switch
the patient into a mixed state?
Because the risk of suicide ishigher in patients with bipolar
mixed state.
Now, there is no solid data,which shows that this is the
(08:16):
reason why there's an increasedrisk of suicide, right?
There's a different hypothesis.
So in 2004, I think, so the FDAactually put the black box
warning they updated in 2007saying that depression itself
can actually increase the riskof suicide But I think like the
good, the best practice isactually to educate the patient
24 years or younger about therisk of switching to mania.
(08:37):
And also to educate the familymembers, because when patients
become manic, they have noinsight.
So it's always a good idea toinvolve the family member.
Talk to them about the risk sothat if the patient misses it,
at least the family members canpick it up.
Dr. Amayo (08:49):
That's a good point with it being that younger of
age, maybe there's more of abipolar components to it, and
that would make sense as to whyit's specific for that age group
that, that we see that risk asopposed to older.
But then I wonder if, becausewomen tend to develop, manic
disorder later in life or whatare, if they're risk for
(09:10):
suicidality, Is a little bitmore extended than males.
I don't know.
Dr. Handratta (09:14):
We don't know that exactly.
Because another hypothesis isthat the patient who is
depressed and is suicidal tobegin with, and as the
depression gets better, thereare more energy actually now to
actually complete this.
So there are differenthypothesis, but none of these
hypothesis has been proven.
Dr. Amayo (09:26):
Yeah, sir.
And then lastly Why do nauseaand vomiting?
I think that's the most commonside effects with our regular
antidepressants.
How about that?
Dr. Handratta (09:36):
So why do we develop nausea?
So the, so there are differenttypes of serotonin receptors
right?
So there's one group ofserotonin receptor called five
HT three receptors, five HTthree, which is basically an
ionotropic receptors It's not aG-protein couple receptor.
So these five HT three receptorsare located in your gut.
As well as it's present in theblood-brain barrier.
So when you stimulate them, itusually stimulates nausea,
(09:58):
vomiting, and headaches.
That's the same reason when youare actually using
chemotherapeutic agent forcancer.
What the chemotherapeutic agentdoes is that it usually
stimulates the antichromaffincells in the duodenum to produce
a huge amount of serotonin Whichserotonin.
Which will stimulate the five HTthree receptor causing nausea in
patients receiving chemotherapy.
Oh, and that's why you have fiveHT three antagonists like
ondansetron So these areactually used for nausea because
(10:18):
they block the five HT threereceptors.
Dr. Amayo (10:21):
And because of their inotropic.
Is that why they work so fast asopposed to the, the typical two
to three weeks before we see thedesired effects we want from
antidepressants.
Dr. Handratta (10:30):
Exactly.
Ionotropic receptors are fasteracting because they are iron
controlled receptors rather thanG protein, which basically uses
a second messenger system.
Dr. Amayo (10:39):
And then I always comfort my patients telling them
that that, the nausea andvomiting will get better after
five to six days.
So do, does this ionotropic fiveHT three receptors get
desensitized to it?
Dr. Handratta (10:52):
So the theory behind actually, when you use
antidepressant for a long periodof time They'll desensitize
these five HT three receptors.
That's when nausea and vomitingdisappears.
After about a week or two weeks?
Sometimes, actually, if it'sreally bad, I sometimes actually
add a five H three antagonist tothe antidepressants so they can
tolerate it better, and aftertwo weeks I slowly take them off
it.
But just make sure that whenyou're giving an antiemetic
(11:13):
agent always makes sure toeducate the patient about
dystonia Especially of the jaw,actually, patient can tell a
dystonic reaction, so it's agood idea to actually educate
them.
But they do develop tolerance toit.
Dr. Amayo (11:24):
Dystonia.
I wasn't tracking that.
Let's talk about it on the nextepisode.
Okay.
Thank you guys and we'll see younext time.
Katrina (11:35):
Thank you for joining us on today's episode.
our tireless team is alreadyhard at work, cobbling together
another potpourri of fascinatingdiscussion for next week, so be
sure to tune in, visit ourwebsite and our podcast feed and
let us know your thoughts on theepisode.
Subscribe so you don't miss ourreleases every Wednesday.
Until next time, keep smiling,keep shining, and stay curious.
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