Episode Transcript
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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 (00:10):
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 (00:20):
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 (00:47):
Welcome back to the Y
in psychiatry.
It is your host, Dr.
Amayo, CL fellow and I'm herewith...
Dr. Handratta (00:53):
Dr.
Handratta.
Dr. Amayo (00:55):
Yes.
And so today we are going to betalking about depression but
we're gonna be talking about thealgorithm of depression.
So it dawned on us that we cameoff firing.
We talked about the neurocircuitry related to depression.
We talked about the fun newdrugs, ketamine and
vortioxetine.
And today we are gonna slowthings down and start from the
(01:18):
top.
And our first question is, whyshould we treat depression?
Why do we exist?
To treat depression asking allthe tough questions.
Dr. Handratta (01:30):
The reason we
treat depression is because we
know depression causes adecrease in the quality of life,
both for the patient as well asthe caregiver.
Depression also can make younon-compliant, especially if you
have comorbid medicalconditions.
Or your medical condition thathas led to comorbid depression.
(01:50):
Depression can actually decreasethe compliance with the
medication, physical therapy, aswell as recovery after surgery.
Plus depression is also a riskfactor.
Untreated long-term depressionis a risk factor for the
development of dementia.
Dr. Amayo (02:02):
Do we know why?
Dr. Handratta (02:03):
The reason being
is that in depression, we know
there is an increase in thelevel of stress hormone that we
call as glucocorticoids, andwhen the glucocorticoids are
increased.
There is a glucocorticoidresistance in depression.
The glucocorticoid can actuallyhave adverse effects on your
brain, which we call as neuraladaptation, so it causes a
decrease in the dendritic spinesin your prefrontal cortex and
(02:27):
hippocampus, and increase in thedendritic spine in your limbic
area like amygdala, so yourlimbic area becomes
disinhibited.
So the prefrontal cortex has nolonger control over your limbic
system.
And when you have loss ofdendritic spine in your
hippocampus, that can lead to alot of cognitive impairment.
Dr. Amayo (02:46):
And this is because
of that state of elevated
glucocorticoids.
So if someone has like Cushing'ssyndromes, do they have similar
risks to dementia?
Dr. Handratta (02:54):
So patients with
Cushings syndrome, we know more
than 50% of them suffer fromdepression.
Plus, Long-term elevatedglucocorticoids does lead to
cognitive impairment in patientswith Cushing's syndrome.
Dr. Amayo (03:05):
All right.
Basically why to treatdepression?
It improves quality of life.
If they have other comorbidissues, the depression, having
depression reduces theirfunction and reduces their long
term.
Prognosis.
And then the big one, which Ithink about for our patients and
even us is it having depressionincreases your risk of dementia.
(03:26):
In the long term.
And that's because of theincreased in gluococorticoids
leading to reduction ofdendritic spines in the frontal
lobe and increase of dendriticspine in the limbic system.
Okay.
And so the next then is justsimple How do we diagnose?
Oh, we are, I think hopefullyeveryone listening to this
podcast know how to diagnosedepression.
Hopefully everyone has studiedtheir DSM fives, TR but what key
(03:50):
takeaway would you say we shouldknow for diagnosing depression?
Dr. Handratta (03:53):
So it's easy to
diagnose depression, right?
So you have to just follow theDSM criteria, or you have the
PHQ nine.
So I believe in using scales.
Because scales helps you todiagnose it.
Plus it also helps to see howthe patient is responding to the
treatment, whether it'spharmacotherapy or
psychotherapy.
once you diagnose depression,few things to keep in mind is
(04:13):
that we have to rule out bipolardisorder, Because if you look at
the data, a patient who visitsprimary care physician,
according to the data out ofevery five patients who have
been diagnosed with depressionin a primary care clinic, one
will have undiagnosed bipolardisorder, So it's missed.
And plus most of the patientswith bipolar disorder, presents
with depression.
(04:34):
So it's extremely importantactually to look at the risk
factors for bipolar depression,as well as doing a mood disorder
questionnaire, which we call asM D Q.
Or you can actually usesomething called as a rapid mood
screener.
So rapid mood screener is ashorter version.
And has a very good sensitivityand specificity.
So if they are positive, thatmeans that there is an increased
(04:55):
likelihood of bipolar disorder.
So you have to go in depth, Ifit's negative means that the
patient doesn't have bipolardisorder so then you can move
forward.
Then you also have to rule outcomorbid medical conditions that
can cause depression.
Like for example, Cushings orpatients who have chronic
conditions like cancer,rheumatological condition, which
causes cytokine induceddepression, Because you have to
(05:15):
treat the underlying conditionfor the depression to get
better, or you have to alsotreat the depression
simultaneously to improve thecompliance with treatment,
right?
Or the medical condition.
Another thing we commonly missis diagnosing sleep apnea.
A lot of times we ask questionsabout sleep, but we forget to
ask about sleep apnea.
untreated sleep apnea can causedepression, So that is something
(05:39):
to look for.
And then ordering basic labslike cbc, cmp, urine toxicology,
thyroid function, vitamin b12,folate, vitamin D, and if
appropriate, ordering R P R andH I V, depending upon the
patient population.
Dr. Amayo (05:55):
Does obesity increase
your risk for depression?
Dr. Handratta (05:57):
yes, so there is
a good question.
So there are some studies whichtalk about obesity.
So your adipose tissue producesabout 30% of inflammatory
cytokine called interleukin six,which can cause something called
"sickness behavior" and thedifference between cytokine
induced depression.
(06:18):
And major depressive disorder isthat cytokine induced depression
is mostly associated withanorexia and psychomotor
retardation.
And there is less feeling ofguilt involved in cytokine
induced depression.
But yes, obesity can increasethe risk of depression, so stay
away from medications that canincrease weight gain.
Dr. Amayo (06:36):
Okay, so key pearls
for diagnosing depression.
Biggest thing, rule out bipolardisorder.
And the MDQ' and the RMS.
Are those free?
Can you like Google them, getthem?
Dr. Handratta (06:48):
Yes you can.
Dr. Amayo (06:49):
Okay.
Good scales to use.
Quick scales with highsensitivity to help you rule
those out.
Keep note of medical conditionswhich can mask as depression or
would not get better if youdon't want depression.
And one big one is obesity andsleep apnea.
Those seems to be missed.
And obesity causes more likelycytokine induced depression with
(07:09):
interleukin six elevation.
And then get your basic labs.
And that would also probablyhelp with the hypothyroidism,
which is another medicalcondition that can present as
depression.
Dr. Handratta (07:19):
That's right.
And Dr.
Amayo I have forgot aboutsubstance use disorders and
medications that can inducedepression like high dose of
steroids, long-term use ofsteroids can cause depression.
So we need to look at that aswell as benzodiazepines can also
cause depression.
Okay.
Yeah.
So you have look at medicationinduced depression as well as
substance induced depression.
Dr. Amayo (07:38):
Okay.
So I think we have why to treatand we have how to diagnosis or
things to keep an eye out forwhen we are diagnosing
depression.
Let's go to, How would you treatdepression?
What's your first line?
First line medication fortreating depression.
Dr. Handratta (07:53):
So the first line
medication for treatment or
depression.
Dr. Amayo (07:56):
Ketamine.
Dr. Handratta (07:56):
Hahahah, I wish
actually that was the first line
treatment, right?
Yeah so the first line treatmentof depression still is SSRI as
well as SNRI.
And these are age oldmedications.
A lot of them actually work verysimilar to each other except the
side effect profile, as well asthe way they are metabolized in
the body, So that those are thedifference But the mechanism of
(08:16):
action of most of the SSRI andSNRI are very similar to each
other.
Most of the SNRIs will work likeother SNRI.
SSRI will work like other SSRIs.
Now, if the patient does notrespond to these medications,
then you can also usevortioxetine.
Which is a newer generationantidepressant, which is not
(08:37):
like a me too ananti-depressant.
It works in a very differentmechanism.
It does hit the transporter, butit also hits the postsynaptic
receptors.
Dr. Amayo (08:45):
And if you subscribe
to our channel, you would've
learned about vortioxetine inthe last episode.
You mentioned if SSRIs or SNRIdoesn't work, how would you know
when they're not working?
Dr. Handratta (08:56):
So again, we do a
PHQ nine at baseline.
Okay?
So we know what our baseline PHQnine scores are, and then when
you use this antidepressant atan optimal dose like for
example, escitalopram, likeanywhere between 10 and 20
milligram citalopram actuallybetween 20 and 40 milligrams or
sertraline between 100 and 200milligrams, right?
(09:18):
When you use it at a goodtherapeutic dosage, in about two
to four weeks, you should see atleast a 20% improvement in your
PHQ nine scores.
That actually has a moderatepositive predictive value that
this patient is going to respondto this medication when you
continue the treatment foranother six to eight weeks.
We are looking for remission,70% improvement in those
(09:38):
symptoms.
Suppose that your PHQ nine scoreis less than 20% improvement in
about two to four weeks at anoptimal dose that has a very
strong positive predictive valuethat the medications aren't
gonna work.
So it's a good idea to switch toanother treatment, which could
actually be from an SSRI to anSNRI or from an SNRI to an SSRI.
(10:00):
Or if you have used both of themeither to vortioxetine or
Bupropion or mirtazapine.
So you can actually like switchbetween the class.
Dr. Amayo (10:08):
Okay.
So first line treatment fordepression, SSRIs or SNRIs and,
get a PHQ nine.
See if in two to four weeks,let's say 20% decrease in
symptoms, if not, seems likeit's most likely that they
wouldn't respond to that.
especially depending on theirsymptoms and how severe their
dysfunction is.
Maybe that would be time toswitch to either to a different
(10:30):
class, SSRI, SNRI, orvortioxetine or bupropion or
mirtazapine and what would beyour second line?
Dr. Handratta (10:37):
So suppose I
started SSRI and the patient
does not respond either becauseit's not effective or because of
the side effects.
Then I usually switch to anSNRI.
That's my second.
And if they do not respond to anSNRI due to it's not effective
or side effects, then Ibasically use Vortioxetine.
Okay.
Because you need to try an SSRISNRI before the insurance
(10:59):
company can approvevortioxetine.
I also use vortioxetine if aperson has depression and also
has some cognitive issues.
Because we know that accordingto research data, vortioxetine
helps with cognitivefunctioning, though it's not FDA
recommended for improvement,cognitive symptoms.
Okay.
So I want people to realizethat.
So it's not FDA approved forcognitive dysfunction.
(11:20):
And if they fail to respond tovortioxetine, then I might
actually use bupropion.
More effective for patients withdepression, with comorbid
nicotine use disorder.
Okay.
Smoking cigarettes, or they alsohave comorbid ADHD where
Bupropion can be used as anoff-label treatment.
And if they don't respond tothat, then I can actually go to
mirtazapine.
But with mirtazapine the problemis weight gain.
(11:41):
Yeah.
And as we spoke, weight gain canactually increase the risk for
depression.
And plus can also makeobstructive sleep apnea worse.
Dr. Amayo (11:48):
So mirtazapine would
probably be good for someone
that has the anorexia, symptomswith their depression.
So maybe it's for someone with,cytokine induced depression?
Dr. Handratta (11:57):
You can use that
actually mirtazapine you can use
in cytokine induced depressionif the patient is losing a lot
of weight.
Yeah, definitely.
You can go with mirtazapine.
And we'll talk about each SSRIwhere it can be used.
Like what's special aboutdifferent SSRIs and SNRIs.
Dr. Amayo (12:11):
I think that's all we
have for today in The Y in
Psychiatry.
So we talked about why to treatdepression.
We talked about how to diagnosedepression.
Don't forget about bipolardisorder.
Don't forget about sleep apnea.
Don't forget about obesity.
And we talked about first lineSSRIs, SNRIs, and if that
doesn't work, you can tryvortioxetine.
It's also bupropion andmirtazapine, depending on the
(12:33):
patient presentation.
Thank you all.
Dr. Handratta (12:36):
Thank you all.
Now we are ready to actually goand eat some meatballs.
Katrina (12:42):
Thank you for joining
us on today's episode.
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