This content is a rapid review session designed to help individuals prepare for board specialty certification exams, focusing on high-yield, core knowledge and exam-relevant concepts across various medical disciplines, particularly in endocrinology and infectious diseases.
Mind Map
انقر للتوسيع
انقر لاستعراض خريطة الذهن التفاعلية الكاملة
All right. Well, welcome everybody to uh
the first session of the rapid review
course for basically BPS exams. So,
anybody studying for one of the board
specialty certification exams um can
attend. And uh this first session is
open uh to everybody including the the
public. So, we're glad to have you. If
you are not a customer of ours, that's
okay. We're still glad to have you.
hopefully you'll benefit. If we can be
of any service to you, uh, please let us
know, but we're we're glad to have
anybody that's on, uh, people are still
logging in. And so, I'm just going to do
a quick introduction. Uh, I'll start off
with myself. If for some of those of you
that are new to us, uh, my name is
Anthony Busty. Um, I got a unique
background. I trained as a nurse, a
pharmacist, and a physician. I currently
practice in emergency medicine.
And uh my role in the company is
editor-inchief. I did also start the
company. So that was 15 years ago. Been
doing this for a long time. Bring a lot
of unique perspectives and background.
So I'm looking forward to interacting
with you guys during this series. Dr.
Koko, why don't you go next?
>> Hi, my name's uh Craig Koko. I'm a
clinical pharmacist and clinical
toxicologist. Uh also work here at High
Yield Medviews. It's been really kind of
an enjoyable process kind of continuing
my uh teaching from you know directly
just pharmacy but you know expanding it
into this realm. Uh it's been really
enjoyable especially again learning from
Dr. Bustai a lot uh myself and then kind
of carrying it forward and try to carry
on that teaching.
>> Dr. Boland.
>> I'm Dr. Cassie Boland and I come from a
unique background although all of it is
within pharmacy. So did a little a
little stint in the ER. There's fun
stories there, but that's for another
time. And uh anyway, so a little bit in
the ER, did some impatient infectious
disease work, uh went back to residency,
went into ambulatory care, been in
academia, and uh I enjoy teaching. I
love teaching and helping others grow
professionally. And so this is a
wonderful opportunity for me as Dr. Kio
uh said as well to uh kind of
carry on the torch of teaching from
here. Absolutely. So hopefully you guys
see that we've got some experts who have
have extensive amount of experience in
different backgrounds, acute care,
chronic care, outpatient, you know, uh
critical care environments. We're going
to have a number of other experts that
will join us for other sessions
specifically like oncology. We have two
clinical uh oncology pharmacists from
University of Kentucky uh Dr. Buts and
Dr. Travers who will be joining us in
that session. So, a lot of exciting
things happening here and a lot of good
people that are going to give you some
great pearls. Now, before we get started
uh with this session, I want to lay a
little bit of the uh rules and the
perspective that we're going to be
coming from. The goal at this point as
we approach exams is that this is not
meant to be primary teaching. All right?
I can't say that enough. We are not here
to dive into the minutia or details. The
goal here is to help you to keep your
mind on this on the focus of the exam.
The again, we talked about this in some
of our reviews on how to pass the test,
but you need a board exam mindset, which
are you need to know the core knowledge,
things that are facts and that are
standards of practice for everybody
across the country. you not splitting
hairs over geographic variations in
practice, not new emerging data, not
cutting edge clinical discussions.
That's not what this is about and nor is
the board exam really about that either.
And that may be surprising to you, but
that is the that is the reality. They
have to be able to an ask you questions
on on standards of care and practice
patterns that are well accepted and well
established. That's what we're going to
hit on tonight, okay? and in this series
of sessions that we're going to be doing
for you. Okay, so we're going to hit the
high points because again the assumption
is you've come in already have had done
some review probably listened to
lectures probably done some practice
test questions or practice exams and now
you just need to you know really brush
off the cobwebs make sure you got
everything as you head into this final
leg in preparation. It hopefully will
also help you to identify any areas of
weakness. Okay. And you may rec you
might want to jot down a note or so of
topics that you want to go back and look
at. For those of you that are customers
of ours, you know that you have a a lot
of material that you can access,
individual lectures on core topics even
of advanced pharmarmacology reviews, but
also disease state reviews and more
depth than what we're going to do
tonight. You have evidence-based
medicine, bioatistics, pearls, and we're
going to cover that later in another
session. But you've got access to those
things. And then of course you have the
more important thing which is practice
test questions over and over and over
again to where you develop that endurance
endurance
and the ability to maneuver from one
topic to another. Unfortunately your
questions on the exam are not going to
be categorized like the next five
questions will be on the topic of
infectious disease. I mean it's going to
be you know you got sepsis on one
question the next question is a
statistical interpretation of a a
metaanalysis you know a forest plot and
then you got to move on to practice
management question then over to you
know indocrine you've got to be able to
mentally maneuver between topics because
that's the reality of the exam that
you're going to be taking regardless of
the specialty exams either you got to
maneuver within your specialty so if
you're in the cardiology group critical
care group ID group, okay? Because I
know that some of you may be
representing different uh exams by
coming here tonight. Uh because we're
talking about endocrine and infectious
disease topics on the other days that
are listed on the website. We'll be
talking about those topics and I'll
summarize those at the end. So, it's
going to feel like a fire hydrant. This
is also not meant to be the time where
you try to jot down every little note.
Really, you should be stopping and just
listening. Think through this as we go
through it. Okay. Should be making sense
to you. You should be able to go, "Yep,
yep, yep." Now, if when we get to a
point, you go, "Yes, but
what about this scenario? We're not
going there." And the reason is is
because it's nine times out of 10 never
going to make it to a board exam. Okay?
We're hitting the most common high yield
core concepts. Okay? So again, I just
wanted to make sure that we were all on
the same page before we get started
because it's going to be a rapid review.
That's the only way we can get through
these topics. One last thing before we
start, we will have a somewhat scheduled
break. Okay, this is approximately a
2hour session. We will save about 30
minutes afterwards for Q&A. So if you
have questions or you want to go back
and hit a topic or you need some more
clarification, save it for then. Okay?
Okay, I'm not going to we're not going
to entertain questions along the way.
We're going to save it to the end. So,
we'll take about a five or 10 minute
break halfway through. Let you stretch
your legs. Make sure nobody gets a DVT
or decubinous ulcer. All right.
So, I don't want anybody claiming that,
right? If you start having a seizure,
just give yourself four milligrams of
Adaban IM. You'll be fine. Okay. All
right. I'm just kidding. Right. We got
to keep learning fun because this is
this is a lot of material and it's hard
and who wants to just have somebody just
mundane boring reading a slide to you?
That's not what we're going to do here. Okay.
Okay.
Alrighty. Well, hopefully you're excited
now and ready to go. Got your drink and
your notes. So, let let's go ahead and
jump in because we're going to hit
adrenal disorders. Okay. Both where the
adrenal gland works too much and not
enough. So Addison's disease D deficient
D deficient. So when you think about the
pathophysiology, we got a reduction in
the ability of the adrenal gland to make
enough cortisol eventually or depending
on what's causing that problem. You may
also impact the amount of aldoststerone
release, which is your mineralorticoid
activity that's really the more profound
impact on sodium and potassium. So when
we think about patients and their
clinical presentation because you got to
know some of that basics because that's
what we're treating is the underlying
problem. You need to think about they're
weak. They have weight loss because
they're deficient in the thing that
causes to retain u volume. Okay. Sodium
water reabsorption is and so they can
develop orthostasis from lack of plasma
volume. Hyperpigmentation of the skin.
Classic. Again, when you're reading a
question on a board exam, you should be
seeing a pattern of association and they
usually give you the diagnosis, but you
should it should be consistent so you
know which drugs to use. So, you measure
these levels, you see the cortisol level
is low. When you do your BMP, basic
metabolic profile or CMP, comprehensive
metabolic profile, you traditionally see
the manifestation of not having enough
mineral corticoid activity, right? So,
you're not reabsorbing enough sodium. So
your serum sodium levels are low and
you're retaining potassium by not
kicking it out when you re reabsorb the
sodium. So you have low sodium, high
potassium, low plasma volume
orthostasis. It then begins to make
sense. So then what do we want to do?
Well, correct the deficiency. Give the
very thing that you're deficient in
which is hydrocortisone. Okay,
hydrocortisone has that balance of
gluccocorticoid activities as well as
mineralocorticoid activities. Okay, we
know that they differ in the steroids,
but hydrocortisone is the drug of
choice. The reason you see plus or minus
fluocortisone has to do with whether or
not you need more potent
mineral activity. Do you need to retain
more sodium and kick out some of that
potassium? The only way you're going to
know that is by initiating the
medications and seeing what happens in
their labs. The non-farmacologic
treatment is TED hose. Those are
basically like tight panty hoes so that
when they stand up, gravity doesn't just
cause all their plasma volume to fall to
where they get laded and dizzy. Now, the
way we're going to function here is that
Dr. Cookio and and Dr. Bolan will
intermittently add to and so I'll just
pause here for a second, but as we go,
they're just going to interject. Okay.
Um, so I'm just kind of leading us
through the disease state. Is there
anything else that you guys want to add
as we move forward?
>> No. All right. Good.
>> Okay. Okay. Well, just jump in when you
do, okay? Because we we will have
moments to to pause. Okay.
>> So, let's think about the crisis level.
So, now you take an Addison's disease
>> and now you are so deficient that you
now have a s systemic problem, right? Or
you can't react to it. a situation like
a stressor, trauma, you know, infection,
particular things like sepsis, you know,
some other s major surgical procedure.
Now remember, that's a stress response.
Our body responds to it. But if you're
dependent on medication and you don't
accommodate that stressful situation,
then the patient can have more profound
basically deficiency symptoms, right? So
they become even more hypotensive, uh,
weak, more severe hypocalemia and
hyponetriia. And so in these cases, you
know, and I'm sure Dr. Kokio can jump in
on this as well, but you need to
supplement them, right? And the answer
is IV hydrocortisone, not PO, IV. Okay.
And you're going to be dosing this, you
know, around the clock. Now, Dr. Koko,
are you any comments about the dosing
based on the stressor?
>> Yeah, so I mean definitely this is
different dosing than you might see in
other indications and it's typically on
the higher end. Uh especially if you can
identify exactly what's going on, but I
mean you can see a range here being 25
to 100, but typically I mean empirically
I guess you could say it would certainly
at least start at 50 milligrams every
six hours which is certainly opposed to
other indications you're going to see
hydrocortisone use. on a clinical exam
if even if they said you know try to
paint a context it's like trying to
reconcile what exactly are they using
this hydrocodone for adrenal crisis
would immediately come to their mind to
try to consider exactly why they're
trying to consider this in in this
clinical context we might also see it in
sepsis but if you loop it back it's
actually somewhat similar considerations
we're taking in that patient population
to exactly what's going on here
>> and just so you guys know from a board
exam perspective dosing because you Dr.
Koko just mentioned that that there is
many there's no standard for like
scenario you you will have to make a you
know patient specific adjustments and
considerations but there's no like oh if
they have you know if they have like a
uh car accident and they have one broken
bone the dose is this right I mean it it
does vary why which is why you see a
range but the idea is to replace it now
let's go to the other side now you're
making too much right so your your g
your your um your adrenal glands are
doing that too much. Most commonly we
see that the the pituitary gland in the
brain is sending a message to your
adrenal glands saying hey make more of
this stuff and the feedback loop is not
really talking to itself. Remember in
all endocrine there's usually this sort
of negative feedback system where one
system talks to another and organs kind
of regulate each other. Well in this
case they're making too much. So now you
got to think of the opposite. you don't
have hypoalmia, you have hypervalmia or
to increased plasma volume where they
have increased blood pressures. Um you
have increased you know gluccocorticoite
activity happening. So of course then
their their glucose levels are high um
because of the edema and the fluid
accumulation they they have weight gain.
Um they obviously have dysipidemia and
then um high levels of steroids we know
cause uh bone mineral density decreases.
So you measure these you see elevated
cortisol uh you see um hyponetriia hypocalemia
hypocalemia
um and again that's because you know
you're excreing so much that you're
sorry that should be hyperremia I think
yes um you know you're you're
reabsorbing a too much uh sodium and
you're now kicking out more of the
potassium so most of the time this is a
tumor cancer problem and so the
treatment is treat the underlying
problem. Well, you might need to provide
them some stability before they go to
surgery. And some drugs like modane,
ketoconazol, materone, those may be used
basically to block some of the
production of those ketoconol being an
antifungal agent, but block some of the
cytochrome P450 isoenzyme systems that
produce some of those or uh hormones.
And so, um, so anyway, it's it's just
one of those treatments, but surgical is
going to obviously be the underlying,
uh, problem. So, which, uh, kind of just
changing up a little bit and and adding
another little pearl here that may
potentially show up, you know, which
sedative hypnotic, you know, some people
call it anesthetic depending on the dose
and how you use it, is known to increase
the risk of adrenal insufficiency. So,
think of it in the context of rapid
sequence intubation. The answer is
automodate. All right. So, it can block
some of that uh enzyme production that
would make uh cortisol. So, you can see
that. Just a quick few comments about
gluccocorticoids because this is a huge
drug class that extends across multiple
indications and uses. Obviously, some
agents are used for other conditions
over some other drugs. Uh I I put an
asterisk ne next to the ones that are um
have less mineral cortical activity and
are longer acting. So that's your
betamethasone and dexamethasone in
particular. Um pretty much devoid of
most mineral cortical activity but have
more they're more potent and so you
don't have to give as much and they have
a longer duration of activity. When we
look at indication, it's obviously
pretty widespread. You know, acute COPD,
uh, asthma, allergic reactions including anaphilaxis.
anaphilaxis.
Um, you got, uh, CROO, especially with
your, um, betamethasone and as well as
your uh, orbinide and and you got uh,
dexamethasone, which are sort of your
drugs of choice to reduce that subglotic
edema. U, you got gout, you got
rheumatoid, osteoarthritis, and
sometimes it's just a small dose. that's
all they need. Um even to the level of
nausea, vomiting. Okay. I mean using it
for that. I mean some like typically
outside of the norm that we think about
but it is used in space patients that
are resistant or not responding to other
anti-imetic therapies. And then
obviously also vasculitic therapies like
temporal arteritis is a classic
indication for highdose long-term use of
steroids. Well, obviously when you use
steroids, you can induce Cushings like
effects, right? And depending on which
ones have more mineral corticoid
activity like predinazone,
hydrocortisone, prediniscolone, they're
going to retain more of that sodium and
water. Um, they're going to potentially
also have an impact on the blood
pressure, which can certainly tip people
over into heart failure. Avascular
necrosis of the hip is typically seen on
higher doses around that predinazone
equivalent of 20 milligrams or more. Um
and that can be devastating and result
in the need for a hip replacement. Um
but and then you have your
gluccocorticoids like dexamethasone,
betamethasone which are going to have a
little bit more effect on those glucoses
and I'm sure Dr. Bolan can you know
comment about that but I mean I see this
stuff wreak havoc in a diabetic. In
fact, I make sure I don't really try to
use these drug drugs in that patient
population if I can, especially if
they're not well controlled.
Um, and then certainly septic shock. Um,
>> yeah, and certainly if you see somebody
who has been treated with
gluccocorticoids for a long time, it
actually presents a different treatment
scenario. So, uh, in which your oral
medications, your GLP-1s, SGLT2s,
uh, not the GLP1s are oral, but just in
general, your non-insulin therapies tend
to not work as well. So, usually these
patients who are on like long-term
gluccocorticoids will end up needing
basilbis like pretty much right out of
the gate when it starts or or fairly
quickly, more than what you would expect
for like a type two, for example.
>> Yep. Uh, another little quick pearl here
that again is board exam um relevant is
what dose of predinazone equivalent
basically is uh to the endogenous
production of cortisol every day. Uh and
and if you read the literature you'll
see a variation but but the most common
number cited is about 7 and a half
milligrams. Once you've achieved that
dose on a daily basis you are now equal
to the amount that your body makes. And
so when you exceed that 10 milligrams,
15 20 milligrams a day, you are going to
cause HPA suppression where if you've
been on it for several weeks, those are
the patients that you definitely need to
uh taper. All right, moving on to hyperlddostroneism.
hyperlddostroneism.
So now you're making too much
eldoststerone and it's usually
independent of the uh renin. Well,
that's would be primary. So like the
gland is just making it not responding
from renin release from the jxogar cells
of the nephron. Um and if you have
secondary causes that is sec uh
secondary would be things like outside
the adrenal gland that is causing
eldoststerone uh to be released in the
context of renin. So think about
hypoprofusion of their kidneys. Uh we
see this a lot in patients with cerosis.
Uh they have low onotic pressures. They
hypoprofuse the JG cells. JG cells in
the proximal renal tubule of the nephron
start releasing tons of aldoststerone
and basically that's what causes the
ascites over time. So what do we give
highdose spironolactone right? So many
of times these patients have refractory
hypertension. You start one or two
agents they don't respond very well. Uh
but many times what you're seeing is you
know their electrolytes being uh off. So
they're going to have a significant
amount of of um sodium. So they're going
to be more hyper natriic with hypocalemia.
hypocalemia.
They're not going to be responding to
anti-hypertensive medications. That
should clue you in. And then if you do
an aldoststerone renin ratio, you see
that it's pretty high, especially in
primary. Um and in those cases, uh the
treatment is straightforward. If it's a
adrenal gland problem like a tumor then
it needs to be resected right if it's
not or it's secondary and something else
is turning on like in cerosis heart
failure and these things then you have
aldoststerone antagonist so you got
anything uh there for you guys
>> yeah I think as you mentioned just kind
of reiterating it's not necessarily for
this but the the spirnolactone to
ferosomoside ratio that the patients
would actually need is somewhat again
it's a dosing question but I think
that's a unique dosing question for
these patients where it would
specifically be 100 milligrams to 40 of
spinolactone to firosomide so the doses
might increase from that perspective but
to me that would be something that could
be you know addressed or inquired upon
in that exam setting
>> absolutely he that 100 to 40 is in the
context of cerosis
>> right exactly Absolutely. Yes. So, so
just you know again the way we use these
drugs um and if you think about even
cerosis we don't use a plurinone the
data is not there it's spernolactone
whereas in heart failure it's
spernolactone and a plerone in much
lower doses >> right
>> right
>> just other little pearls make sure you
avoid uh salt substitutes with potassium
in them that's a good counseling point
for your outpatient patients on heart
failure meds where you're treating them
uh chronically uh because a lot of times
they'll replace the sodium with potassium
potassium
And then the gynecomastia with
spernolactone is clearly a problem
especially for men. All right.
Fiochromoscytoma. Now the adrenal gland
is making too much catakolamine. Okay.
Um and when you make too I we're talking
about catakolamines, norepinephrine,
epinephrine. So what do you think
they're going to present like? Well,
they're going to have palpitations. What
is epinephrine doing? It's stimulating
those beta 1, beta 2 receptors. What is
norepinephrine doing? it's it's
stimulating uh maybe some of the beta 1
receptor but predominantly hitting that
alpha receptor right so you're seeing
blood pressures going up you're seeing
uh the sweating palpitations
these types of things um and then if you
when you do an exam or evaluation you
you basically collect the urine and you
look for uh these metaneprins in the
urine and the plasma and that helps you
to get the diagnosis the part of the
problem is you go okay well they're
making too much catakolamine but where's
the tumor
So it can be not only in the adrenal
gland but some of them can be outside of
the adrenal gland. And so that's where
imaging modalities are implemented so
that you can find the tumor so that the
surgeon can go in and essentially remove
it. However, most surgeons and
anesthesiologists and the rest of the
crew, they don't want to take patients
back to the O with unstable pulses and
unstable blood pressures. And that's
where other drugs are being used to
control their blood pressure. So you got
oral phox phoxybenzamine which is
available orally uh not fenolamine which
is more your printal agent. Uh other
options that are available oral that are
commonly used are docazisonin tzisin. I
mean, you can put them on drips around
the time of surgery as they become NPO,
but you're basically treating them with
a lot of drugs that would reduce the
afterload from all the stimulation of
the alpha 1 receptors in particular. All
right, moving on to endocrine. Again,
hopefully you guys are finding that, you
know, again, we have to kind of move
through these things fast. It's rapid
fire, rapid review. So, not to insult
anybody's intelligence here. That's not
the goal. I know that most people
attending this probably have a good
understanding of type one, type two, DK,
and you know, gestational diabetes. So,
we'll kind of move through some of these
fast, but just as a reminder, uh
obviously type one is autoimmune. U just
realize that some patients can go
through a phase where as they're
autoimmune, destroying their pancreas
and beta cells, they may still make some
insulin. Um and it just depends on when
you are seeing them. Okay. Uh but
obviously a lot of times DKA's uh I'm
sorry, type ones will present and if
they don't have a diagnosis, it's
usually at the time that they develop
DKA, something gone wrong. They're they
show up with the classic findings. Um
and when you do more specific lab work
outside of the DKA, which we'll talk
about here in a minute, you clearly see
that they're, you know, fasting blood
sugars are over 126, their hemoglobin
A1C is over 6 and a half%. If you do
just do a random glucose, they're
usually over 200 with the three Ps.
Polyura, polyypsia, polyphasia. That's
usually um happening at the same time.
So our treatment for type one
chronically, Dr. Boland, walk us through
this. This is your baby, right? Hit the
high points. It's like straightforward,
but there are there's no oneizefits-all.
>> No, not at all. Um so there first of all
you're going to do basilbis and as Dr.
Busty mentioned some patients will make
some insulin so you may even have a type
one who doesn't even require insulin for
a brief period. So but in general what
you're looking for is a basilbis regimen
with about 50/50. Uh clinically you
might see 6040 one way or the other. Uh
some patients are even stable on 7030
but again that's that's thinking more
clinically. Uh but if you're trying to
figure out this out from the get-go,
you're looking at a total daily dose of
that 0.4 to one units per kilo per day
and then you divide that out 5050 and
then of course you divide your prenial
insulin usually into those three doses.
Uh pumps and CGMs should absolutely be
considered. Uh you I I can't imagine
that a board exam is going to ask you
about a specific pump. uh but they could
potentially give you some basil rates
maybe or or a correction factor or a
carb factor or something like that and
ask you you know kind of what would you
adjust uh especially with the emphasis
that they're starting to put on CGMs you
I would say you want to look at one of
those reports familiar familiarize
yourself with those numbers but with
diabetes whether it's type one or type
two kind of a test taking strategy for
you is if they start talking about
something really specific for a patient
they really this care is very patient
specific. So if they start giving you a
lot of individualized patient
characteristics, you need to start
really thinking through some of these
things and are they trying to get you
towards a pump, things like that.
>> Yeah. And that probably shows up more in
type two where you have, you know, this
insulin resistance pattern. You're
depending on what stage they're in,
their pancreas is uh and their beta
cells are pumping out like tons of
insulin. And then over time as the beta
cells burn out you begin to migrate into
basically becoming essentially insulin
dependent at some point if you don't
intervene on the underlying causes. Uh
some of these patients will have changes
in their weight weights. Obviously their
lab findings are very similar to um uh
patients with type one and then as Dr.
uh Bol and I'm going to let her like
jump in here, but what you see on here
are some of the things that guide us to
patient specific choices and there are
so many factors that go into that, but
I'll let Dr. Bolan highlight the key
points here before we move on.
>> Yeah. So, u it's sort of trending now
towards what we've or at least I've been
doing in practice for a while. A lot of
people have been doing but metformin is
still generally considered your first
line treatment, but you do have some
wiggle room there. Now again for those
patient specific factors um to choose
something different uh if it is again
good for the patient. So now we need to
consider ASCVD if they have a history of
that, if they have a history of heart
failure, they have a history of CKD, uh
you have different pathways for those.
Even considering cost initially or
access um that all of those things are
now taken into account when choosing
your initial drug therapy, which
metformin is still a great initial
choice. But again, if you start hearing
ASVD or, you know, events and heart
failure and CKD, then you need to start
thinking about uh, you know, for your
GLP1s, ASVD or CKD,
SGLT2s, ASVD, your heart failure for
sure, uh, and CKD. Um, and then weight
loss, you're going to think about your
GLP1s, SGLT2s, metformin, uh, and then
DPP4s. If you're just looking for
neutrality, um, across the board and not
to cause any additional gain. And then
if you're if they're really pushing cost
and there are some other factors in
there that are pushing you, you can go
with sulfonal uras, uh, or TZDs. So
really, you've got to if they're giving
you a case, you've got to look at the patient.
patient.
>> Yeah. I mean ghost go glaburide just kid
right I mean but here's the deal met
Metformin and some of these drugs are
cost-effective options and and they do
have some supporting data so and we're
going to come back to some of those
things here in just a few minutes we got
a few slides where we dive into a little deeper
deeper
>> uh about some of the SGLT2s as well as
the GLPS so we'll come back to this in a
second gestational diabetes obviously
during pregnancy there are obviously
changes in insulin resistance that
sometimes can be asymptomatic but you
see it. Um and so we actually screen uh
patients for this by doing oral glucose
tolerance tests. I guess some of these
patients can go on and have in a
post-natal period um gestational
diabetes uh that extends and results in
diabetes especially if the if the female
doesn't obviously lose uh their their
their weight. Now we start thinking
about um some of the agents that can be
used in um uh pregnancy that have been
studied. Metformin and glaburite
actually have been studied have been
used are some are okay to consider. Uh
clearly the preferred agent is insulin
and the whole idea behind this is to
really try to make sure that baby
doesn't get too big because it's got a
hole to come out of right and if it gets
too big it gets stuck. And I've
delivered babies many times, sometimes
emergently. Don't like to do that, but
you don't want a baby getting stuck.
Okay? Uh that's a sometimes a medical
emergency. So push you back in, just go
to the O, right? Uh but let's move on to
some of the more life-threatening
situations that you guys could be at.
For those of you doing the acute care
side, um even those of you in the
ambulatory care, you need to be able to
recognize the complications of a chronic
medical illness because they come in and
out of the hospital system. So this is
where your insufficiency of insulin is
such that now you've caused a
derangement in the metabolic u you know
factors your your biochemistry at the
cellular level where you are producing
keto acids usually in many cases um or
you get such high levels of glucose that
you not only volume deplete the patient
but you also cause electrolyte
deficiencies. both cause electrolyte
deficiencies because the kidneys just
cannot handle all of the glucose that
are is is spilling. The threshold is
exceeded which is around 180 milligrams
per diliter. You just start dumping it.
Well, what follows sod glucose water.
Well, what follows what's also in that
water in the urine filtrate?
Electrolytes. So, you start to have a
significant amount of dehydration,
electrolyte abnormalities, poly
polyipssia, polyasia. Um, and when you
do labs, then you start seeing that an
gap metabolic acidosis. And you don't
have to have, especially in DKA, blood
sugars that are, you know, 6 800. In
fact, there typically are around less
than 500. Um, you'll see them just above
250. HH um S or HS,
you don't necessarily see ketosis or
necessarily on GAP, but you can see
sugars that are 800, 900, over a
thousand. I mean, I've had patients
with, you know, 1,500 u milligrams per
deciliter of blood sugars. I mean, it
just they're so severely dehydrated uh
when they show up. And so, volume
resuscitation in both patients is very
important. Now, there's also a level of
resuscitation that you don't want to go
too high because you could cause
cerebral edema if you, you know, push
fluids too fast, especially in our
pediatric patients. But you also need to
consider electrolyte placement
especially before you ever give these
patients insulin. And that is a take-home
take-home
definitely point that must be made. >> Absolutely.
>> Absolutely.
>> Yeah. Go ahead, Craig. I mean, jump
right in.
>> Oh, yeah. No, I mean this is one of
those key things where the
differentiation here, the key therapies
for DKA or HHS is not insulin.
>> Absolutely not. That's a third like I
mean, in my mind, it's third line. So
you do fluid resuscitation, um you do
electrolyte replacement and you
absolutely have to make sure that
potassium is replaced before you start
insulin. Like those are key factors
almost guaranteed to be on the exam if
you see a a patient case in this
context. I mean almost guaranteed. Um
even still like with crystalloid uh the
selection of a crystalloid might come up
because a normal saline if you give too
much of a high volume again too quickly
you start to in introduce the you know
possibility of hypercchlormic metabolic
acidosis and you falsely eliminate that
gap before you actually clinically
eliminate the gap of the patient. So
there's you know other balanced
electrolyte or crystalloids that can be
substituted instead of normal. It seems
so simple but like def definitively
clinically relevant and also def
definitively elements on a on an exam
where that case might or the clinical
question might actually prompt you to be
able to select the the actual correct answer.
answer.
>> Yeah. And and just so you guys know, you
will you most patients are on insulin
drips in these situation and you will
start to put them on a dextrose
containing infusion around that 250
milligrams per deciliter because you're
trying to feed the cells and reverse the
system and then you won't really
actually let them start eating until
you've closed the gap.
>> Okay, that's when you know you can begin
that transition to subcutaneous insulin
and now let them uh let them eat. um
hypoglycemia. Uh you have um you know
maybe too much insulin um and not enough
glucose or the way you do the insulin
and the patient didn't eat. So their
kinetics didn't line up right. Um these
patients obviously can present in a
number of ways but classically altered
mental status. They can even have
seizures. They can even have stroke like
symptoms. And that's why when patients
come in with a stroke the one of the
first things we check is the glucose.
Okay? when they're having seizures, we
check the glucose. You just have to
treat the underlying cause. And so,
don't forget that that can happen. Uh,
Whipples triad basically is when they
come in with symptoms that are
suggestive of hypoglycemia like the
above and they're usually their glucose
levels are 55 to 60 or less. Um, and
then when you give them glucose, it's
almost like they miraculously come back
to life. It's I mean, it's amazing.
Watch it happen right in front of you.
So your treatments in mild cases as long
as they're maintaining their airway and
they're not seizing and they're not
gurgling in their saliva. Uh you can you
know do like you know glucose uh gels or
tablets. These things there's kind of
the rule of 15. Give 15 grams of oral
glucose. Check them their acue check in
15 minutes. You should see about a 25 at
least milligram per deciliter increase.
And if you don't go ahead and give them
some more. But if they're altered and
they're not controlling their airway or
secretions, it is parental dextrose like
D5 or D10 uh I'm sorry, D10 usually or
amp of D50 even uh depending how low it
is. And uh or if you have no IV access
and you can't get it in, just stab them
with glucagon.
Like literally stab them.
>> Now recognize that that you know the
glucon isn't going to last forever. Now
diabetes and cypitus, there's two types.
This is really more related to uh a
problem with anti- diiuretic hormone and
there's the central and then there's the
nephrogenic central is that the brain
from a number of reasons usually trauma
traumatic brain injury or encphylopathy
from we see this sometimes in patients
postcode if they survive with ros or
tumor uh where they're making too much
antidiuretic hormone and basically um
they're just retaining all this free
water Okay. Uh so they're having anti-diaresis.
anti-diaresis.
So it goes to the collecting tubules and
basically reabsorbs free water. Uh
nephrogenetic is when the kidney itself
is failing to respond to u the
antidiuretic hormone. So you'll see uh
variations um in the problem, right? Um
and so if you have the you know
nephrogenic where they're not responding
and and they they're just dumping free
water then they may be excessive
urination u and that's kind of typically
what we you know we'll see. So you do
plasma and urine osmolalities and look
at their uh sodiums and try to help
define what the problem is. So desmopressin
desmopressin
uh is more for central and uh uh
nephrogenic diabetes and cypitus is you
try to treat the underlying problem. Now
desmopressin is also used for other
conditions um and they're important to
recognize uh one of them being that you
might potentially see on the boards is
uremic platelet dysfunction or uremic
bleeding u is the drug of pretty much
the drug of choice in most situations uh
when you encounter that. Okay Dr. Bolan,
walk us through quickly uh some of this
emerging information that probably is
now uh testable with GLP-1 agonist and
SGLT2s that you kind of alluded to
earlier. Give us the key points here.
>> Yeah. So, just to kind of look at both
of these drug classes for CKD and we'll
talk about them for the others as well,
but first for CKD, you're looking for
reduced EGFR below 60. Um, and you know,
there may come some dosing questions
there with, you know, different
creatinin clearance, whether you're
using it for heart failure or CKD. Um,
so just be aware of that. Make sure you
kind of freshen up on those because
those can change a little bit. Um,
again, so as I'm saying that again, they
may not put that on the board because
that is somewhat inlex with the
different uh indications and things like
that. So anyway, um you're going to look
at their urine, album, and creatin.
Think about that. Your SGLT2s are
probably your go-to for CKD. Uh they
have the most evidence, but then your
GLP1s come in with some uh additional
evidence there. Uh and you can choose
those second line. Um so those trials
have really been limited by just lack of
a standard renal outcome. So that was
kind of the bold print bold print there.
really hard to compare. Uh so in
thinking about cardiovascular risk
reduction, your GLP1s,
uh they all have demonstrated safety
andor superiority. Um they uh so you've
got gelaglatide, luraglletide, and
simaglletide subq that have shown
superiority and carry indications. So
you want to know to use those for ASCBD.
Um and dulaglatide actually has a
primary prevention indication. So if
you've got a patient that's high risk
but has not had an event, dulaglatide is
the one you're going to choose. Um and
then with the SGLT2s and ASCBD,
canagloin and impagloin are the ones
that have demonstrated some superiority
with the three-point mace. So those
would be the ones that you would choose there.
there.
uh in heart failure. Um this one is
interesting in some ways, especially for
SGLT2s. With the GLP1s, it's been
secondary outcomes. So, they don't have
a primary outcome trial yet. So, that's
not going to be uh your choice. However, clinically,
clinically,
you certainly have evidence there that
you could choose one if the patient was
not a candidate for SGLT2s if they had
heart failure. Uh so for SGLT2s and
heart failure they as a class in general
they have demonstrated reductions in
heart failure hospitalizations and
death. So if you've got a patient with
heart failure you need to start thinking
SGLT2 and is it appropriate because
there are a lot of adverse effects with
these medications that could make it not
appropriate and that may be what they're
trying to get you around to as well. Um
so depacen and impactloin have primary
evidence in both patients with and
without diabetes for heart failure. So
that's also important. So if they have
heart failure, they don't have diabetes,
you could potentially still be looking
at an SGLT2 if it's appropriate.
>> Perfect. All right. Insulinoma making
too much insulin. There's a tumor and
just by the name makes sense. So these
patients present with severe usually hypoglycemia
hypoglycemia
sometimes very difficult to control.
When you measure insulin levels or
cpeptide levels they're pretty high. You
got to go looking for the tumor because
basically the treatment is surgical
resection. The one of the drugs of
choice that has been around for decades
is dazoxide. It's an old thazide
diuretic. And just as a quick side note
you know thyide diuretics we know do
increase glucose levels. And if you look
at epidemiologic data, patients on
thyide diuretics tend to have a little
higher incidence of hypoglycemia or even
diabetes. So dazoxide being in that
class is an oral option for that.
Everlymus is another option. Um it's an
mTor uh antioplastic agent. So it's
treating the cancer that's producing the
insulin itself. Obesity obviously when
you have excessive caloric intake and
not enough expenditure. By definition,
that's a BMI over 30. Remember, 25 to 29
is overweight. Um, something else to
keep in mind when you're talking about
obesity is the waist circumference
because these put patients at sort of
that higher risk of coorbidities. Um,
but a lot of times they will um show up
in a triad. you see hypertension, hyper
lipidmia, they start developing insulin
resistance or the metabolic syndrome
especially if it's that visceral
atyposity uh you know the dunlaps
disease um so treatment is the no duh
yeah yep exercise I know I know it's
hard uh but exercise and diet um now if
you start to get to where those things
are not options because it's not
necessarily the case for everybody then
there are some emerging therapies that
have come out. Um the fentamine and
fentamine com combined with the
antic-convulsant topyramate or topamax
um nal trexone bupropion combination
larglutide and then even surgical
interventions where patients you know
get lap bands and different things like
that uh which have pros and cons as
well. So none of these things in and of
themselves or by themselves are
standalone. Okay. So SIADH this is
usually a patient with uh uimmic
hyponetriia. They probably have a little
bit too much free water because of a
little bit too much excess antidiuretic
hormone. They usually present
non-specific. they're just kind of eh
don't feel well, you know, and you start
running some basic labs and you find
them to have hyponetriia with some
changes in their in their urine sodium
um and osmolerity that kind of guide you
to it. So really the treatment the
easiest first line treatment is free
water restriction. I mean slam dunk that
is it. Okay. If somebody has severe
hyponetriia, you know, whether then then
you got to start thinking outside of the
box where you need to be careful with
the correction and you might be using uh
sodium chloride, you know, replacement
therapies where you're going to be
limited by how much you can administer
over a 24-hour period to reduce the risk
of central pontine myinitis. But that is
usually in patients uh with more severe hyponatriia.
hyponatriia.
You can use the vasop prein agents like
tolvaptan for resistant cases but moving
on. All right. Thyroid disorders we have
hypo and hyper and then we have the
extreme. So in hypo that's mixedoma
uh or mixade edema. Uh this is where
they're not making enough T4. Okay. And
this may be you you know your TSH levels
are really high but there's something
wrong with the gland. And so the output
of T4 and eventually then T3 is now compromised.
compromised.
So think about low metabolic demands. Um
and these can vary on the severity or
the the amount of T4 that is not
present. But most of these patients are
tired. They feel depressed. They're
gaining weight. They have cold
intolerances. When you get to mixedadema
comomas, you start having breda cardia,
paricardial fusions, altered mental
status, severe hypothermia. The so they
vary in based on the uh levels. So when
we screen for hypothyroidism really what
we most usually screen for is TSH and it
is usually elevated. If you have an
elevated TSH but a normal T4 that is
considered subclinical hypothyroidism.
Okay. But when both the TSH is high and
the T4 is low that is clinical um or
overt hypothyroidism where patients need
to be on replacement therapy and the
drug of choice is synthetic T4
uh therapy and you recheck that at
approximately six to seven weeks. Okay,
I repeat that. It's a good question.
When will steady state for that dose be
achieved? Six to seven weeks. Um, and so
you got to be careful with making dose
adjustments too quickly because
eventually that patient will have a
steady state level that will be too
high. The halflife is about seven days.
So it makes sense. Now there's a comment
down here that says avoid T4 T3
combinations in most patients. Those are
really reserved for patients who do not
have the ability to peripherally convert
T4 to T3. Uh because when you give fixed
combinations, you're forcing the patient
and their genetic profile to that amount
of T3. Whereas when we give synthetic
T4, your body doesn't know and the and
the peripheral deodinase
doesn't know where it came from. So it
will convert what it needs from T4 to T3
and T3 is more potent or metabolically
active. So allow the body and the body's
own genetic profile metabolic demands
drive that. Dr. Koko, anything mixed
edema that we need to make sure these
guys know.
>> Yeah, absolutely. So I mean agent
selection as you were emphasizing here
would be uh T4o levothyroxine is the the
key therapy here. The the caveat that
though is that it can't be administered
uh orally or entrally uh for those
patients because in that clinical state
their GI absorption is almost absent
entirely. So although again in pharmacy
realms we often try to do a PO to or IV
to PO conversion in this situation it's
absolutely they they need parental
levothyine. Again, a dosing concept
here. Again, I don't think it's
irrational to kind of consider the
dosing because it can range quite
severely from anywhere from a 100
micrograms all the way up to essentially
a milligram. But there's clinical
evidence not to definitively say which
one is the best, but it is relatively
high compared to where you would start
somebody on hypothyroid hypothyroidism
with a relatively low levothyroxine dose
and then titrate up.
>> Excellent. Okay. So what is the average
dose increase in levothyroxine
uh dosing in women with who have known
hypothyroidism and get pregnant and
they're in the first trimester and the
answer is up to 48%.
So and it so at the time of diagnosis uh
many of the guidelines and position
statements recommend a 30% increase
almost immediately and then you may need
to further increase that all the way up
to 43 to 48% um depending on what you
read. So it is a significant increase
during pregnancy and the early that so
you reduce the risk of miscarriage and
uh you know you don't impact negatively
neuro neuro development. All right. Now,
let's go to hyperthyroid.
You make too much T4 or too too much T3.
Um, in many cases, you have the
opposite. You have weight loss, right?
You have sweating. You have
palpitations, your energy, you know,
maybe even uh increases in temperature
or fevers. Um, the extreme and
thyrotoxicosis, again, changes in mental
status. They may be even having a panic
attack, agit being agitated, they can go
into atrial fibrillation. Um, so it is
the opposite. So hopefully those two
sort of make sense. So you would see low
TSH because the brain is receiving too
much feedback from all the T4 T3. Um,
you can use some uh scoring uh
diagnostic criteria like listed here.
Um, if we're looking for thyrotoxyosis,
but a lot of times you know it based on
clinical exam and you can get some basic
labs and you can figure that out. So for
hyperthyroid states until you can remove
the thyroid gland so thyroid ectomy uh
these patients get put on uh methmosol
or PTU. Dr. Koko run us through real
quick thyrotoxicosis key points.
>> Yeah. So uh key points here again these
patients again just exists on an
extreme. So although most of the drug
therapy is actually still relatively
similar. So uh MMI or PTU they would get
started on initially. Um we're actually
trying to treat them um very acutely in
one rational state. There's a lot of
somewhat caveats that you might consider
here. But one of the the key ones at
least in terms of uh what I try to
consider is a the
iodine administration. So either SSKI or
lugalls that you have there. Um and
again they are drops. They're kind of uh
tissue toxic if you don't dilute them.
So they have to be diluted before
administration in almost every scenario.
And then propranol there's some uh
situations here where propranol has been
extensively demonstrated that it can
actually uh definitively kind of prevent
the conversion of t uh you know
producing more T43 in those clinical
scenarios. Many other beta blockers
really haven't been able to demonstrate
that. There is some emerging evidence
with ethmol as an alternative uh just
because proprrenol does have a very long
duration of action. Essol is entirely on
the opposite side. And again here also
you see uh you know cortosteroids uh
essential uh to that administration too.
So the the drug therapy does expand to
at least four of those uh key therapies.
So MMI or PTU plus SSKI or lugalls uh
and then plus beta blocker plus plus
aortic steroid. So it gets fairly
complex and then uh those patients
>> you're basically based on how they
respond you know. So just keep in mind
on the peripheral conversion of T4 to
T3, you're blocking it with PTU and propanol.
propanol.
>> And when you're inhibiting the release
of it from the uh you know stimulation
from from the gland and uh peripheral
conversion, those are your steroids. So
you're hitting it, you're trying to hit
the process from multiple angles. What
medication is known to contain high
concentrations of iodine and can cause
hypothyroid states? Amiotarone. 37% of
each dose of amiotarone is iodine and at
some point you super saturate uh the
gland and it starts to shut it down. All
right, moving on to parathyroid
or hyperarathyroid. This is remember
your parathyroid hormone depending on
the concentration can have different
effects. Um patients can um it regulates
the calcium homeostasis from the bone.
It also regulates how much is absorbed
in the GI tract, how much is released in
the in the kidneys. So you got to keep
these in mind and they the parathyroid
glands sit behind the thyroid itself and
so when you do a thyroidctomy you
actually have to dissect out the
parathyroid glands and put them back
into the body. Um so really what happens
you we got to watch out for patients who
develop hyper uh um hypercalcemia and
hypocalcemic states depending on the
level of functioning of the of the
parathyroid hormone that is is present.
Um and so you like I said you can see
persistent hypercalcemia with elevated
uh PTH which is a primary condition
where they have uh parathyroid adenomas
most commonly um and hyperlasia and then
hypocalcemia from secondary. So again
there's a it almost seems
counterintuitive at some level but you
need to recognize that it's a dose
related effect that's happening on
different organ systems. So if you have
somebody with hyper calcia and they have
that stones, bones, groans and
psychiatric overtones from too much
that's IV fluids, IV fluids, IV fluids,
that is the treatment of choice. Um if
you have a secondary cancer like a
problem that's like metastatic disease
to the bone and it's causing
hypercalcemia malignancy then in those
cases those are patients getting usually
on a bisphosphinate and it's a single
dose of pomeigronate or a single dose of
zolandronic acid because it it takes
about a week for the full effect of that
to happen. Some people will use parental
use of calcetonin if the IV fluids don't
work. But what you don't see on here is
Lasix. you can add Lasix to the regimen
of high dose of IV fluids if they need
to get rid of the extra volume. So,
people with high risk of heart failure.
Um whereas if you're hypocalcemic or you
have the secondary causes, then you may
actually need to be giving them calcium
um um replacements. Okay. So, moving on
to some infectious disease and then
we're going to take here take a break
here in a in a few minutes. Um we're
going to move on to an soft tissue
infections in this group. Okay. So
animal bites, human bites. Animal bites,
uh, bad. Human bites also bad. Uh, but
especially cat bites because they
they're fangs and they can inoculate and
puncture the wound, which we not only
have bacteria on our skin, but they have
bacteria in their oral ferings and they
basically inoculate it and they can
inoculate it pretty deep and most of the
time it's in the hand. So you're talking
about joints. Hand infections get bad
fast. Um, so be very very careful. So
the most common place is the extremity.
Next is the face and the neck because
people put their faces up next to
animals and they reach up and and bite
them. Um so high risk of infection needs
good wound irrigation and deb brement.
Um these patients need to be put on drug
of choice augment clavulonic acid is the
drug of choice for both animal and human
bites. So remember that if you have
animals, tetanus, well for animals in
Houston, tetanus is both because I mean
our mouths are dirty. Um and people that
get into certain types of bar fights and
things may be really dirty. Uh but you
also got to keep in mind rabies. So if
you don't know the uh vaccine status uh
of the animal, they can be quarantined
and monitored by a vet, but the only way
to diagnose if the animal has uh rabies
is to basically kill the animal and do a
biopsy. Uh so it's it's you know you you
got to do that because getting rabies
can result in permanent uh neurologic
damage. And so you do have a little bit
of time before you give the rabies
immune globulin and the vaccination. And
by the way, when you if you do have a
dog or an animal that is suspicious for
rabies, when you are cleaning the wound
and you know doing the repairs, you have
to inject the rabies immune globulin
literally around the bite marks all over
and then whatever is remaining you put
in the same arm or clo you know a more
proximal from away from the wound. Um,
and a lot of people don't realize that,
but you're injecting literally
antibodies all around it if you have
that high of suspicion. Humans, I can
gota be real careful with these um,
organisms. Um, most of the time it's a
fight. So you, you know, punch somebody
in the in the face, it hits the teeth,
it gets right there in the knuckle, it
gets septic joints. Bad news. Bad ruse.
That's why you see these third, fourth,
metacarpalangial joints because of the
the bar fight, the punch. That's usually
uh where it happens. And again, these
infections can be bad and the hands can
swell up and many times have to go to
surgery to have that washed out. So
wound irrigation early, clean it. We
don't always sew these up to be honest
with you because we want the ability of
the organisms to get out. If we sew them
up and suture them too tight uh then we
can trap those bacteria in and again
treatment of choice augmentin augmentin
augmentin and then tetanus. All right
moving on to feliculitis. Think of it
hair follicles. So when you look at them
these patients come in and they have
kind of red spots all over the place um
and around the hair follicles usually in
that distribution. Uh the history is
important. Uh sometimes, especially if
you're considering sudamonus, uh if
they've been exposed to lowcllorinated
uh pools or hot tubs or whirlpools, if
that's in the case, that's what they're
trying to get you to think about. But
think about what's the most common on
the skin, staff orius, strep species.
You see these red areas around the hair
follicles and they form these little
pestules. Um and so most of the findings
are based on exam alone. Sometimes you
can do wound cultures, but quite
honestly, by the time you get that
information back, the patient's going to
be, you know, have already been treated.
So with mild cases, you can get away
with topical mupin, but if it's
involving a larger area, obviously you
can't coat your whole body with mupin
ointment. I mean, you can just slip
around um all over the place. Uh but
it's also not reasonable or feasible. Um
and that's where systemic antib uh antibiotics usually things like KLEX are
antibiotics usually things like KLEX are the most common used. All right, moving
the most common used. All right, moving on to cellulitis. This is an infection
on to cellulitis. This is an infection involving the epidermis and dermis and
involving the epidermis and dermis and starts to spread within the superficial
starts to spread within the superficial fascia. So it's not going deep in the
fascia. So it's not going deep in the myofascial planes yet. Um they swelling,
myofascial planes yet. Um they swelling, inflammation, a local area of redness,
inflammation, a local area of redness, fever. Sometimes you can see streaking
fever. Sometimes you can see streaking uh or track marks going away from the
uh or track marks going away from the area of infection. You can also see
area of infection. You can also see lympadnopathy in the same extremity. Uh
lympadnopathy in the same extremity. Uh again where fluid would be draining.
again where fluid would be draining. Key differentiation from a syipolis
Key differentiation from a syipolis nonelevated lesions that would be on a
nonelevated lesions that would be on a board exam whereas irrious you're going
board exam whereas irrious you're going to see well demarcated uh level
to see well demarcated uh level elevations of the uh infection itself.
elevations of the uh infection itself. Okay, two scenarios.
Okay, two scenarios. If you have an abscess IND, many times
If you have an abscess IND, many times IND alone in a patient with no
IND alone in a patient with no co-orbidities,
co-orbidities, no significant risk factors, no known
no significant risk factors, no known colonizations of MRSA can be effectively
colonizations of MRSA can be effectively treated with IND. Period. That's it.
treated with IND. Period. That's it. Okay? No need for antibiotics in those
Okay? No need for antibiotics in those situations. If you start getting
situations. If you start getting patients with other co-orbidities that
patients with other co-orbidities that put them at higher risk, especially
put them at higher risk, especially imuninompromised states and diabetics,
imuninompromised states and diabetics, you definitely want to consider adding
you definitely want to consider adding on emperic therapy to that. And you
on emperic therapy to that. And you know, you see those listed here, clinomy
know, you see those listed here, clinomy basically being reserved for the
basically being reserved for the penicellin allergic patient. Um if you
penicellin allergic patient. Um if you um are concerned about MRSA then those
um are concerned about MRSA then those patients may need to have anti
patients may need to have anti antibiotics that cover for a
antibiotics that cover for a specifically more community- based MRSA
specifically more community- based MRSA that would be your backrum
that would be your backrum trimethropoxol
trimethropoxol or docycl
or docycl is overkill
is overkill um and you're only using venkcomy really
um and you're only using venkcomy really if the patient is being admitted because
if the patient is being admitted because they're septic uh usually from it. Now,
they're septic uh usually from it. Now, aeric syphilis is now not only the
aeric syphilis is now not only the superficial dermis, but it's now
superficial dermis, but it's now spreading and it's spreading rapidly and
spreading and it's spreading rapidly and it's going through the lymphatic system
it's going through the lymphatic system where when you look at the findings,
where when you look at the findings, they have this uh demarcation around the
they have this uh demarcation around the edge. It's like I mean you can just see
edge. It's like I mean you can just see the line. It looks like a big bully
the line. It looks like a big bully that's just moving and splitting the
that's just moving and splitting the surface of the skin. Um, and these
surface of the skin. Um, and these patients get pretty sick and it's very
patients get pretty sick and it's very painful uh for them. But the drug of
painful uh for them. But the drug of choice is penicellin. Penicellin.
choice is penicellin. Penicellin. Penicellin. Now you can also use not
Penicellin. Now you can also use not only penvk if they're if it's a mild
only penvk if they're if it's a mild case and you can treat them as an
case and you can treat them as an outpatient but also amoxicylin or even
outpatient but also amoxicylin or even kellex if they're being admitted to the
kellex if they're being admitted to the hospital
hospital ancef or spazzin
ancef or spazzin uh or uh vank and if they're especially
uh or uh vank and if they're especially if they're penicellin uh allergic neck
if they're penicellin uh allergic neck fash this is the life-threatening
fash this is the life-threatening medical emergency this is a rapidly
medical emergency this is a rapidly progressing necrosis basically of the
progressing necrosis basically of the myofascial plane pains. So, it's gone
myofascial plane pains. So, it's gone deeper and it's moving and within hours
deeper and it's moving and within hours this patient literally could be dead.
this patient literally could be dead. Um, and when you palpate this and you
Um, and when you palpate this and you look at their clinical presentation,
look at their clinical presentation, they have crepitus, which means when you
they have crepitus, which means when you push down on their skin, you can
push down on their skin, you can actually feel air like almost like ris
actually feel air like almost like ris rice krispie sensation underneath the
rice krispie sensation underneath the skin. And these patients are severely
skin. And these patients are severely toxic and basically this is a medical
toxic and basically this is a medical emergency. You can use this score here,
emergency. You can use this score here, which is a laboratory risk indicator for
which is a laboratory risk indicator for necrotizing fascia score. But quite
necrotizing fascia score. But quite honestly, if you have clinical suspicion
honestly, if you have clinical suspicion of neck basing
of neck basing stupid labs and waiting to do that test
stupid labs and waiting to do that test that you go straight for a surgeon and
that you go straight for a surgeon and you start them on empiric antibiotics.
you start them on empiric antibiotics. Uh Dr. Kio, I don't know if even Dr.
Uh Dr. Kio, I don't know if even Dr. Bolan, I know you back in the day
Bolan, I know you back in the day inatient and uh and on the antimicrobial
inatient and uh and on the antimicrobial stewardship services. I don't know if
stewardship services. I don't know if you guys have seen this but you know
you guys have seen this but you know surgery needs to be consulted emerently
surgery needs to be consulted emerently you can still start emperic antibiotics
you can still start emperic antibiotics um any thoughts
um any thoughts >> yeah this is where it comes to the order
>> yeah this is where it comes to the order of antibiotics now you can debate this
of antibiotics now you can debate this clinically but there's almost no way you
clinically but there's almost no way you can prove this in a clinical trial but
can prove this in a clinical trial but it's entirely rational in my setting
it's entirely rational in my setting where clinomy has to be administered
where clinomy has to be administered first like so the logic behind that is
first like so the logic behind that is that we're trying to inhibit the toxin
that we're trying to inhibit the toxin production toxin release and uh protein
production toxin release and uh protein synthesis from those cells cells that
synthesis from those cells cells that you're immediately going to lice with
you're immediately going to lice with the piccillant tasabactam. So you need
the piccillant tasabactam. So you need to reduce the endotoxin that's being
to reduce the endotoxin that's being released causing this essential neck
released causing this essential neck fashion. You could uh you can rapidly
fashion. You could uh you can rapidly rapidly make it worse if you don't at
rapidly make it worse if you don't at least try to inhibit those protein
least try to inhibit those protein synthesis and then lice the cells. So
synthesis and then lice the cells. So it's always clinto first which is
it's always clinto first which is deviant from or deviation from standard
deviant from or deviation from standard practice where you do betalactin first
practice where you do betalactin first in almost every situation.
in almost every situation. >> Absolutely. So moving on to fungal
>> Absolutely. So moving on to fungal cutaneous canidasis. We have not only
cutaneous canidasis. We have not only strep staff on our skin but we have
strep staff on our skin but we have Canada um and so we show we see these
Canada um and so we show we see these show up in the oral fingial area and
show up in the oral fingial area and imuninompromised patients. It can show
imuninompromised patients. It can show up on on uh patients with other
up on on uh patients with other coorbidities especially diabetics uh
coorbidities especially diabetics uh warm moist environments in the folds of
warm moist environments in the folds of skin or fat. Um and you we see this in
skin or fat. Um and you we see this in kids with diaper rashes. Many times they
kids with diaper rashes. Many times they can develop this and it just the the the
can develop this and it just the the the local uh skin is just very red and
local uh skin is just very red and extremely irritated. Um once it moves
extremely irritated. Um once it moves and disseminates into the blood
and disseminates into the blood obviously just like with bacteria they
obviously just like with bacteria they have systemic manifestation of fever,
have systemic manifestation of fever, chills can become hypotensive. Um so
chills can become hypotensive. Um so most of the time this is diagnosed based
most of the time this is diagnosed based on exam. So if you have mild cases, you
on exam. So if you have mild cases, you can get away with oral fluconazol or
can get away with oral fluconazol or even topical nestatin and there's
even topical nestatin and there's different formulations. If you're doing
different formulations. If you're doing oral fangial candidasis
oral fangial candidasis um then you can do the swish and swallow
um then you can do the swish and swallow type of mechanism. But fluconazol quite
type of mechanism. But fluconazol quite honestly is probably easier to use. But
honestly is probably easier to use. But if you're talking about topical for top
if you're talking about topical for top nestatin for like diaper rash or
nestatin for like diaper rash or cutaneous candidasis if you start
cutaneous candidasis if you start getting into systemic um you're thinking
getting into systemic um you're thinking about amplitaris B you're thinking about
about amplitaris B you're thinking about econocandons
econocandons uh antifungal agents
uh antifungal agents squirrel tracosis this is basically
squirrel tracosis this is basically where this would show up is a gardener
where this would show up is a gardener working out in their landscaping and
working out in their landscaping and with um rose bushes I mean that is the
with um rose bushes I mean that is the classic presentation they poke their
classic presentation they poke their skin with the rose bush and it
skin with the rose bush and it inoculates sporics into the skin and
inoculates sporics into the skin and basically they it can disseminate and go
basically they it can disseminate and go through multiple organs into the lungs,
through multiple organs into the lungs, bone and joint and eventually into the
bone and joint and eventually into the central nervous system. Um you can do
central nervous system. Um you can do blood in ur uh um sputum cultures
blood in ur uh um sputum cultures especially if it moves into the lungs or
especially if it moves into the lungs or a tissue biopsy but the treatment of
a tissue biopsy but the treatment of choice is itchonazol itconol
choice is itchonazol itconol or itchonazol uh especially if you're
or itchonazol uh especially if you're going to be treating it and the patient
going to be treating it and the patient is stable ampliteration B is obviously
is stable ampliteration B is obviously if they're more disseminated and have
if they're more disseminated and have CNS uh involvement
CNS uh involvement u okay I'm going to stop here after this
u okay I'm going to stop here after this thing here what this last clinical
thing here what this last clinical integration what antibiotics are known
integration what antibiotics are known to inhibit monomine oxidase case and
to inhibit monomine oxidase case and increase the risk of drug interactions.
increase the risk of drug interactions. This is important. It'll show up most
This is important. It'll show up most guaranteed on a board exam, okay?
guaranteed on a board exam, okay? Multiple board exams because we don't
Multiple board exams because we don't think about antibiotics causing a lot of
think about antibiotics causing a lot of major drug interactions, but it's
major drug interactions, but it's lenazalid and tadalid. So, be very very
lenazalid and tadalid. So, be very very careful with that. And with that, we'll
careful with that. And with that, we'll we'll pause here and we'll take a uh
we'll pause here and we'll take a uh five to 10 minute break. So, let's how
five to 10 minute break. So, let's how about this? Let's see. How about we do
about this? Let's see. How about we do about let's meet in the middle? Seven
about let's meet in the middle? Seven minutes.
minutes. Stretch your legs. Get a breather. Get
Stretch your legs. Get a breather. Get that blood circulating. We'll see you
that blood circulating. We'll see you back in seven minutes.
back in seven minutes. See what time is that going to be.
>> All right. Yeah, somewhere around there. All right. Good. All right. I'm gonna
All right. Good. All right. I'm gonna I'm gonna pause for just a second. Turn
I'm gonna pause for just a second. Turn off uh my mic. We'll I'm gonna stretch
off uh my mic. We'll I'm gonna stretch my legs as well.
right, we're going to start back here in about a minute or so. Hope everybody got
about a minute or so. Hope everybody got to stretch your legs, got a drink,
to stretch your legs, got a drink, right?
Hope everybody's uh learning something and feeling like it's,
and feeling like it's, you know, dusting off those cobwebs and
you know, dusting off those cobwebs and helping you to hit those key points. And
helping you to hit those key points. And it's a rapid review. So, uh, we
it's a rapid review. So, uh, we certainly value your feedback as well.
certainly value your feedback as well. And, um,
we're going to stay on at the end here for anybody that wants to ask any
for anybody that wants to ask any questions.
It's a lot of content. Fire hydrant.
Fire hydrant. >> Oh yeah,
>> Oh yeah, >> I wasn't lying about the fire hydrant.
I just didn't tell you how many gallons per minute it was coming out.
per minute it was coming out. It's good stuff. It's good stuff, guys.
I know it is fast, but that's why it's rapid.
Just stay with us. Don't give up. >> Absolutely.
So, don't Yeah. Don't give up, guys. Don't uh you know, feel like, okay, I
Don't uh you know, feel like, okay, I can't, you know, just let it
can't, you know, just let it just sit here and and think through it.
just sit here and and think through it. Here are the key points.
Here are the key points. Get the take-home points at minimum. Let
Get the take-home points at minimum. Let that at least set in. Right? If you feel
that at least set in. Right? If you feel like you need to go back there, you got
like you need to go back there, you got time to still study. That's our goal
time to still study. That's our goal here. All right. All right. So, um I'm
here. All right. All right. So, um I'm going to go ahead and get started
going to go ahead and get started because we still got quite a bit to go.
because we still got quite a bit to go. Fire hydrants open back up
Fire hydrants open back up and uh so hold on to your seats. All
and uh so hold on to your seats. All right. So, bone and joint osteomiitis.
right. So, bone and joint osteomiitis. Okay. So, there's many times there's a
Okay. So, there's many times there's a direct inoculation. That's what we most
direct inoculation. That's what we most commonly think of. We think about the
commonly think of. We think about the diabetic foot or maybe there's some uh
diabetic foot or maybe there's some uh wound where it's close to the bone and
wound where it's close to the bone and it directly inoculates that certainly
it directly inoculates that certainly can happen but it also can
can happen but it also can hematogenously spread UTI STDs pulmonary
hematogenously spread UTI STDs pulmonary infections it gets in the blood it can
infections it gets in the blood it can deposit in a bone period okay and that's
deposit in a bone period okay and that's sometimes sometimes we don't think about
sometimes sometimes we don't think about that um many times it's associated with
that um many times it's associated with an infection that joint if it's
an infection that joint if it's involving a bone you'll see redness and
involving a bone you'll see redness and swelling um and that's where we got to
swelling um and that's where we got to get concerned if there is like a septic
get concerned if there is like a septic joint involved or if there is a wound
joint involved or if there is a wound and the close proximity of that wound to
and the close proximity of that wound to an area. Um but once it's gotten into
an area. Um but once it's gotten into the blood then you have bacteria just
the blood then you have bacteria just like sepsis or anything else. Um now how
like sepsis or anything else. Um now how is the approach to management? We really
is the approach to management? We really need a bone biopsy. I mean that's the
need a bone biopsy. I mean that's the key. Now do you how do you know if
key. Now do you how do you know if someone has osteomiitis? Well I can look
someone has osteomiitis? Well I can look at them and see if the bone is exposed.
at them and see if the bone is exposed. The presumption is they probably do.
The presumption is they probably do. Okay. And I've seen chronic wounds with
Okay. And I've seen chronic wounds with bone exposed decubitous ulcers, foot
bone exposed decubitous ulcers, foot infections from diabetics. That can
infections from diabetics. That can happen. But you may ultimately need an
happen. But you may ultimately need an MRI to make the diagnosis. X-rays do not
MRI to make the diagnosis. X-rays do not give you the diagnosis unless it is so
give you the diagnosis unless it is so slam dunk obvious in which case they see
slam dunk obvious in which case they see perostial reaction. But it's an MRI.
perostial reaction. But it's an MRI. Okay. Now, what do we do? You want a
Okay. Now, what do we do? You want a bone biopsy so they can culture that so
bone biopsy so they can culture that so they can narrow in on the bug. You don't
they can narrow in on the bug. You don't want to swab an open wound that's
want to swab an open wound that's colonized with all kinds of stuff,
colonized with all kinds of stuff, especially if it's in the sacrum because
especially if it's in the sacrum because it's going to be polyicrobial. That
it's going to be polyicrobial. That doesn't help you. And these patients may
doesn't help you. And these patients may be on therapy for weeks depending on how
be on therapy for weeks depending on how it where it's located and how it's
it where it's located and how it's treated. Um but you need to think about
treated. Um but you need to think about the flora that's present on the skin
the flora that's present on the skin versus if it's like in a decubitous area
versus if it's like in a decubitous area then you may see more gram negatives you
then you may see more gram negatives you have to think about that if it's a
have to think about that if it's a diabetic right then you have to even
diabetic right then you have to even think of more polyicrobial even
think of more polyicrobial even sudamonus all right we'll come back to
sudamonus all right we'll come back to that in a minute now I mentioned septic
that in a minute now I mentioned septic arthritis and this is where there's
arthritis and this is where there's bacterial inoculation or spreading into
bacterial inoculation or spreading into the joint space itself so you know you
the joint space itself so you know you see a literally if a joint is swollen in
see a literally if a joint is swollen in red knee, you know, the elbow, the
red knee, you know, the elbow, the finger, any of those joints that are
finger, any of those joints that are common. If you can't prove otherwise,
common. If you can't prove otherwise, that needs to be uh treated and and
that needs to be uh treated and and handled like it's a septic joint. And
handled like it's a septic joint. And these patients have significant pain and
these patients have significant pain and swelling over that. They usually lose
swelling over that. They usually lose range of motion, uh mainly because of
range of motion, uh mainly because of the pain. And the only way you're going
the pain. And the only way you're going to know is stick a needle in it. Yep.
to know is stick a needle in it. Yep. So, make sure they don't punch you in
So, make sure they don't punch you in the face as you're sticking the needle
the face as you're sticking the needle down into the their joint because it
down into the their joint because it hurts. The other thing that you don't
hurts. The other thing that you don't want to do is you want to make sure that
want to do is you want to make sure that you do think there's joint involvement.
you do think there's joint involvement. And there are some exam findings that
And there are some exam findings that you can do like weightbearing
you can do like weightbearing assessments that if it causes pain or
assessments that if it causes pain or it's high suspicion because of a close
it's high suspicion because of a close proximity, then you want to be careful
proximity, then you want to be careful not to introduce bacteria into a joint.
not to introduce bacteria into a joint. So if you have a cellulitis that's just
So if you have a cellulitis that's just superficial and the superficial dermis
superficial and the superficial dermis but not tracking down in the joint,
but not tracking down in the joint, don't boy sticking a needle through the
don't boy sticking a needle through the red skin that's cellulitic and pushing
red skin that's cellulitic and pushing bacteria into the joint. You will now
bacteria into the joint. You will now make a septic joint. So it is a tough
make a septic joint. So it is a tough decision to do it but basically the only
decision to do it but basically the only way to diagnose septic arthritis is to
way to diagnose septic arthritis is to do a joint. So you get synovial fluid,
do a joint. So you get synovial fluid, you see these elevated white blood
you see these elevated white blood cells, PMN's in there. Many times it's
cells, PMN's in there. Many times it's cloudy and based on the location and
cloudy and based on the location and based on the patient's history if
based on the patient's history if they're colonized with MRSA then you're
they're colonized with MRSA then you're going to obviously add uh you know MRSA
going to obviously add uh you know MRSA coverage usually with venkcomyosin most
coverage usually with venkcomyosin most commonly
commonly if it's if it's uh no high-risisk
if it's if it's uh no high-risisk patient uh no histories no other
patient uh no histories no other coorbidities then you can start off with
coorbidities then you can start off with you know ANSF nefaselin those are
you know ANSF nefaselin those are certainly appropriate options If you're
certainly appropriate options If you're concerned about hematogynous and there's
concerned about hematogynous and there's perulent drainage already coming from
perulent drainage already coming from the joint, you need to cover for not
the joint, you need to cover for not only MRSA, but you need to probably
only MRSA, but you need to probably extend the spectrum, especially if
extend the spectrum, especially if there's evidence of sepsis uh going on,
there's evidence of sepsis uh going on, and that's where your sephop and
and that's where your sephop and maropenum would be great options. Now,
maropenum would be great options. Now, diabetic foots infections are typically
diabetic foots infections are typically polyicrobial because they have their
polyicrobial because they have their foot in a shoe and they're usually
foot in a shoe and they're usually dirty. I mean, let's just be honest.
dirty. I mean, let's just be honest. Anybody that's ever seen a diabetic foot
Anybody that's ever seen a diabetic foot infection can smell it from across the
infection can smell it from across the emergency department or clinic and it's
emergency department or clinic and it's very obvious that it's infected. Um but
very obvious that it's infected. Um but that so it's foul smelling. There may be
that so it's foul smelling. There may be even drainage coming from it. Uh you can
even drainage coming from it. Uh you can even see bone involvement. Uh they don't
even see bone involvement. Uh they don't feel it, right? And especially if they
feel it, right? And especially if they step on something uh because they have
step on something uh because they have diabetic neuropathy. Well, they don't
diabetic neuropathy. Well, they don't only not diabetic neuropathy, they have
only not diabetic neuropathy, they have vascular impairment. So they're not even
vascular impairment. So they're not even bringing the precursors to wound healing
bringing the precursors to wound healing necessary to fight the infection and
necessary to fight the infection and heal that wound. So that's why they tend
heal that wound. So that's why they tend to be chronic in nature. So these
to be chronic in nature. So these patients need to have surgical
patients need to have surgical debrement, wound irrigation, and then
debrement, wound irrigation, and then they try to sample the core of that to
they try to sample the core of that to get the actual bug. So many times for
get the actual bug. So many times for providers like me in the emergency
providers like me in the emergency department, I don't start emperic
department, I don't start emperic antibiotics on these patients. I get
antibiotics on these patients. I get them to orthopedic surgery. They take
them to orthopedic surgery. They take them to the O, they do the cleaning, and
them to the O, they do the cleaning, and then they get a bone biopsy from that
then they get a bone biopsy from that source so that they can discern. Now, if
source so that they can discern. Now, if they're going to do an amputation, then
they're going to do an amputation, then the treatment is much different because
the treatment is much different because you remove the infection and the source
you remove the infection and the source of the infection. But sometimes you
of the infection. But sometimes you can't always remove all the bone and so
can't always remove all the bone and so some of that bone remains. And so your
some of that bone remains. And so your treatment is guided by a number of those
treatment is guided by a number of those factors. So, I'm sorry there's no
factors. So, I'm sorry there's no one-sizefits-all answer here, but you
one-sizefits-all answer here, but you definitely need to be considering
definitely need to be considering sudamonus into that picture, especially
sudamonus into that picture, especially if the patient comes into you. And I've
if the patient comes into you. And I've seen this, I can't tell you how many
seen this, I can't tell you how many times, maybe Dr. Boland, you in your di
times, maybe Dr. Boland, you in your di your care clinics that you've been in
your care clinics that you've been in with your diabetics, but I've seen
with your diabetics, but I've seen patients come in here like, "Doc, I got,
patients come in here like, "Doc, I got, you know, I'm bleeding. My sock has got
you know, I'm bleeding. My sock has got blood on it. I don't know what the deal
blood on it. I don't know what the deal is and I like pick up the shoe and
is and I like pick up the shoe and literally like look at the bottom and
literally like look at the bottom and there's the, you know, flat part of the
there's the, you know, flat part of the nail and I look inside the shoe and like
nail and I look inside the shoe and like there's a nail sticking up literally
there's a nail sticking up literally like this and they're just literally
like this and they're just literally grinding it away.
grinding it away. >> I can't tell you how many times I've
>> I can't tell you how many times I've seen that and they're walking on it
seen that and they're walking on it without pain.
without pain. That's how bad it is,
That's how bad it is, >> right? So when you you when you have a
>> right? So when you you when you have a nail through the sole of a rubber shoe
nail through the sole of a rubber shoe that that type of um sole typically
that that type of um sole typically harbors pseudamonus and so you have to
harbors pseudamonus and so you have to keep that in in mind. Dr. Bolan, I don't
keep that in in mind. Dr. Bolan, I don't know if you have any additional
know if you have any additional things you want to say there. If you
things you want to say there. If you don't that's okay. Um,
don't that's okay. Um, >> no, I just think it's important, you
>> no, I just think it's important, you know, and and thinking about you
know, and and thinking about you clinically and for an exam, you got to
clinically and for an exam, you got to think about counseling. Uh, you know,
think about counseling. Uh, you know, what they may ask as far as counseling
what they may ask as far as counseling or what, you know, how you should
or what, you know, how you should counsel someone to take care of their
counsel someone to take care of their feet and when you should do foot exams
feet and when you should do foot exams if they're high risk, if they're not
if they're high risk, if they're not high risk, and things like that because
high risk, and things like that because it is very important to catch early. And
it is very important to catch early. And sometimes I will say they don't even
sometimes I will say they don't even present like these really nasty
present like these really nasty um you know looking wounds that are
um you know looking wounds that are already open and Sometimes they
already open and Sometimes they are kind of internal and coming out. So
are kind of internal and coming out. So it'll present like a callous that just
it'll present like a callous that just all of a sudden they look at it and
all of a sudden they look at it and they're like well it just looks a little
they're like well it just looks a little more red around the edge. Uh and then
more red around the edge. Uh and then you open that up and the you know
you open that up and the you know ulceration is underneath. So it's not
ulceration is underneath. So it's not always this gruesome kind of just you
always this gruesome kind of just you know
know >> that's true very good point.
>> that's true very good point. Hypercaratic lesions or calluses
Hypercaratic lesions or calluses build up tiss uh skin and it pushes down
build up tiss uh skin and it pushes down into it's like a pressure ulcer is
into it's like a pressure ulcer is what's happening. And so literally the
what's happening. And so literally the podiatrist if you ever send a patient to
podiatrist if you ever send a patient to a a foot specialist they'll par and
a a foot specialist they'll par and shave off literally that dead skin to
shave off literally that dead skin to reduce the pressure on that point. But
reduce the pressure on that point. But you can almost see the ulceration
you can almost see the ulceration happening just like Dr. Bolan said where
happening just like Dr. Bolan said where underneath you could transparently see
underneath you could transparently see the blood and the black spots from the
the blood and the black spots from the dead skin and dead tissue from
dead skin and dead tissue from underneath. So you know preventative
underneath. So you know preventative care is key. Dentists, vision,
care is key. Dentists, vision, opthalmologists, podiatrists,
opthalmologists, podiatrists, dieticians, I mean when you're taking
dieticians, I mean when you're taking care of a diabetic patient, it is a
care of a diabetic patient, it is a multiffactorial approach. Moving on to
multiffactorial approach. Moving on to lung infections, bronchitis,
lung infections, bronchitis, virus,
virus, do nothing. No, just kidding. Do not do
do nothing. No, just kidding. Do not do not give patients mucinx. It is
not give patients mucinx. It is absolutely the worst drug on the planet.
absolutely the worst drug on the planet. It makes people cough. It is an
It makes people cough. It is an expectctorant. And people come in all
expectctorant. And people come in all the time, man, I am coughing worse than
the time, man, I am coughing worse than I ever cough. I know because you're
I ever cough. I know because you're taking that stupid drug.
I was just joking, trying to some of you guys up, but the reality is it I
guys up, but the reality is it I everything I said was actually true. Um,
everything I said was actually true. Um, and they should take mucinex off the
and they should take mucinex off the market. It actually has zero clinical
market. It actually has zero clinical benefit, but bronchitis is almost
benefit, but bronchitis is almost guaranteed to be viral or allergen
guaranteed to be viral or allergen mediated. They're smoking. It's a virus,
mediated. They're smoking. It's a virus, right? So, they have this chronic cough.
right? So, they have this chronic cough. It can last more than even three months,
It can last more than even three months, you know, and it occurs multiple times
you know, and it occurs multiple times throughout the year for several months.
throughout the year for several months. It is symptomatic. So, you can give
It is symptomatic. So, you can give antitusive therapies, you know, um, but
antitusive therapies, you know, um, but no antibiotics. That is going to be the
no antibiotics. That is going to be the question on the test. Okay.
question on the test. Okay. Broncholitis.
Broncholitis. >> Dr. Bust, let me just throw in a
>> Dr. Bust, let me just throw in a antimicrobial stewardship point here
antimicrobial stewardship point here with the bronchitis
with the bronchitis >> and the bronchulitis even. So that is
>> and the bronchulitis even. So that is really important when we're thinking
really important when we're thinking about antimicrobial stewardship. A lot
about antimicrobial stewardship. A lot of times we're thinking about big
of times we're thinking about big interventions. Like we're thinking it's
interventions. Like we're thinking it's got to be something, you know,
got to be something, you know, earthshattering.
earthshattering. But this is the kind of question you're
But this is the kind of question you're going to get. Like if they are asking
going to get. Like if they are asking you about antimicrobial stewardship,
you about antimicrobial stewardship, it's going to be about are you choosing
it's going to be about are you choosing the right drug and the right for the
the right drug and the right for the right bug at the right time and you're
right bug at the right time and you're given the right duration. So right here
given the right duration. So right here is very important. So many patients get
is very important. So many patients get antibiotics for bronchitis. It's crazy
antibiotics for bronchitis. It's crazy to even think about. I mean, you're
to even think about. I mean, you're talking like
talking like >> Exactly.
>> Exactly. >> That's what everybody wants. They want
>> That's what everybody wants. They want an antibi an antibiotic solves
an antibi an antibiotic solves everything. Depression
everything. Depression >> solves everything.
>> solves everything. >> Uh your financial problems, um your
>> Uh your financial problems, um your marriage.
marriage. >> I mean,
>> I mean, it fixes everything. Okay.
it fixes everything. Okay. >> Well, and so exactly. And a lot of times
>> Well, and so exactly. And a lot of times we do it for convenience uh and to just
we do it for convenience uh and to just get the patient out of there and give
get the patient out of there and give them what they want. There's some
them what they want. There's some communication techniques you can use
communication techniques you can use there to actually appease the patient
there to actually appease the patient and prevent them from complaining to you
and prevent them from complaining to you versus giving them an antibiotic that
versus giving them an antibiotic that could potentially hurt them. I mean up
could potentially hurt them. I mean up to 25% of patients have GI side effects
to 25% of patients have GI side effects including cediff silk from antibiotics
including cediff silk from antibiotics period. So they're not benign. They can
period. So they're not benign. They can alter your flora for up to even two
alter your flora for up to even two years. So again, just don't. And there's
years. So again, just don't. And there's your antimicrobial stewardship question.
your antimicrobial stewardship question. I love it.
I love it. >> Point.
>> Point. >> So, and the other thing is I'll point
>> So, and the other thing is I'll point out here is a lot of times providers
out here is a lot of times providers will do it for fear because they're
will do it for fear because they're afraid they're going to miss the
afraid they're going to miss the pneumonia. But you've got to remember if
pneumonia. But you've got to remember if if you're not seeing in a patient signs
if you're not seeing in a patient signs of pneumonia, then you've treated them
of pneumonia, then you've treated them properly, you know, in sending them away
properly, you know, in sending them away with without the antibiotics. So be sure
with without the antibiotics. So be sure you do your due diligence there to make
you do your due diligence there to make sure that they don't have pneumonia.
sure that they don't have pneumonia. >> Counsel them. Give them return
>> Counsel them. Give them return precautions if you're if the diagnosis
precautions if you're if the diagnosis is vague and they're not hypoxy. We're
is vague and they're not hypoxy. We're going to talk about commu uh community
going to talk about commu uh community pneumonia here in a second. But
pneumonia here in a second. But bronchulitis is now affecting those
bronchulitis is now affecting those smaller airways and that's usually RSV.
smaller airways and that's usually RSV. An RSV is almost always in the pediatric
An RSV is almost always in the pediatric patient, usually in that two-year
patient, usually in that two-year window, and they just make tons of
window, and they just make tons of mucus, and they just sound horrible. And
mucus, and they just sound horrible. And of course, it scares the parent,
of course, it scares the parent, especially the new parent who doesn't
especially the new parent who doesn't know, you know, anything. Um, they they
know, you know, anything. Um, they they they get all freaked out about it and
they get all freaked out about it and really uh they are they can't be sick.
really uh they are they can't be sick. Um, but most of the time they're going
Um, but most of the time they're going to be fine. And it's self-limiting on
to be fine. And it's self-limiting on its own. You can do a diagnostic work up
its own. You can do a diagnostic work up on them. You can actually test for RSV.
on them. You can actually test for RSV. It helps to give the diagnosis. It all
It helps to give the diagnosis. It all help so helps with the counseling point
help so helps with the counseling point that Dr. Bolan was talking about as it
that Dr. Bolan was talking about as it relates to antimicrobial stewardship
relates to antimicrobial stewardship because again they're going to go why
because again they're going to go why are you not giving my kid an antibiotic
are you not giving my kid an antibiotic because you have a a virus does nothing
because you have a a virus does nothing to that you know and quite honestly it's
to that you know and quite honestly it's suction nasal suctioning the bulb
suction nasal suctioning the bulb syringe depending on the age of the kid
syringe depending on the age of the kid and it's just a lot of suctioning
and it's just a lot of suctioning getting rid of those secretions in the
getting rid of those secretions in the patient who's having maybe wheezing
patient who's having maybe wheezing that's resulting in
that's resulting in uh hypoxia so their pulse oxes are in
uh hypoxia so their pulse oxes are in that low 90 they're real close to 90 or
that low 90 they're real close to 90 or they're hypoxic and needing supplemental
they're hypoxic and needing supplemental oxygen then in those patients you can
oxygen then in those patients you can consider uh nebulized therapies and the
consider uh nebulized therapies and the treatment would be nebulized a
treatment would be nebulized a hypertonic saline bronco dilators really
hypertonic saline bronco dilators really don't do much uh we use them but they
don't do much uh we use them but they really don't use do much and if you got
really don't use do much and if you got sort of selected patient with bronco
sort of selected patient with bronco pulmonary dysplas pies with early you
pulmonary dysplas pies with early you know lung disorders then you can
know lung disorders then you can consider other treatments all right
consider other treatments all right moving on to communityquired pneumonia
moving on to communityquired pneumonia okay strep numo H flu um uh staff
okay strep numo H flu um uh staff klepsiella and then your atypicals
klepsiella and then your atypicals that's your myopplasma pneumonia your
that's your myopplasma pneumonia your chlamyia pneumonia and your legionella
chlamyia pneumonia and your legionella okay newilia that you would consider in
okay newilia that you would consider in those situations u you know again
those situations u you know again they're going to have fever many times
they're going to have fever many times they're going to they may usually report
they're going to they may usually report chest pain because they have an
chest pain because they have an infiltrate and it's irritating the lung
infiltrate and it's irritating the lung parankma it may even be irritating the
parankma it may even be irritating the plural tissue so that when they're
plural tissue so that when they're taking a deep breath or they're
taking a deep breath or they're coughing, it hurts. And again, that's
coughing, it hurts. And again, that's some of the differentiation from
some of the differentiation from bronchitis because bronchitis is
bronchitis because bronchitis is generalized irritation. Whereas
generalized irritation. Whereas pneumonia tends to be localized and it
pneumonia tends to be localized and it infiltrate. And so you do a chest X-ray
infiltrate. And so you do a chest X-ray and if you see no infiltrates
and if you see no infiltrates and it's wide open, looks normal, that's