This content is a rapid review session for BPS exams, focusing on high-yield disease states and their management across gastrointestinal, renal, geriatric, and neurological systems. It aims to refresh existing knowledge rather than introduce new concepts.
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Well, welcome everybody for another
session of the rapid review for BPS
exams. Uh we got a lot uh kind of pushed
in tonight. We're going to try to uh
keep it very uh somewhat focused on the
core disease states. again trying to hit
the highest tier or higher yield u
disease states and you know some of the
therapeutic issues some of the advanced
pharmacology issues that relate to
managing these uh particular conditions.
Um so the idea behind this is not to be
primary teaching. So that's first and
foremost make sure we're on the same
page. Uh we are not teaching this as the
core content. It's supposed to be a
review on top of what you've already
done. Um so we've got several subjects.
Uh thankfully they are a little bit
smaller compared to things like
infectious disease and cardiology which
you know golly there's kind of continues
on and on and on and on. Uh but we got
geriatrics, we got gastronurology, we
got some renal disorders and then uh
neurologic uh disorder. So it's and ger
gerosych or geronuro type things kind of
go together. there's a little bit of
overlap that will happen, not on
purpose, but um we've tried to separate
them into their buckets if you need to
hop off. So, we're going to first start
off with um uh gastrointestinal
disorders. And the way again just as
this occurs, we're hitting the high
points and then Dr. Boland will, you
know, just kind of periodically kind of
jump in and add some additional points.
And so, we'll just kind of go back and
forth. If you end up having questions,
go ahead and, you know, feel free to ask
them depending on how time goes u
because I'm going to be monitoring that
closely since we seem to have a uh it's
too much fun here um and too much
dialogue. But if I can't uh keep it
within the time frame, then we'll wait
till they do the questions at the Q&A
session towards the end. And having said
that, why don't we start off with some
constipation? Hopefully, you're not
constipated. Uh but there's a lot of
reasons that people get constipated. It
can be from mechanical problems
obviously can be from obstructive
problems. Uh it can be also drug induced
and the most common is calcium channel
blockers, opioids, antiolinergic
medications. I mean those are slam dunk.
I can't tell you how many times I see
calcium channel blocker induced
constipation in the emergency department
of all places. Uh but obviously causes
abdominal pain, cramping, bloating. If
it gets bad enough or there's an
impaction, then they start having
nausea, vomiting, and that's a more of a
surgical concern. By definition, usually
these patients are having less than
three bowel movements uh per week, hard
stool straining. So, how do we prevent
that stuff? Well, we soften the stool.
There's stool softeners, but there's
also dietary uh it's not rocket science,
but one thing you also keep in mind is
adequate hydration. As the stool enters
into the large intestine, the idea is to
dehydrate it so that it forms a stool.
So if it sits in the large intestine
longer periods of time, it's going to
get harder and harder and harder. Uh and
so you want to make sure you're
adequately hydrated. So those are the
straightforward things. When we think
about laxatives, we have stimulant
laxatives and then we have sort of these
osmotic, you know, agents like
polyethylene glycol that both increase
the fluid concentration but also
stimulate parastoaltic movements. And
probably Mirillax is one of the more
common um useful agents. And then of
course if it's opioid induced and none
of those things are working. Okay. Uh
then you have your periphery acting
opioid receptor antagonist which are uh
unique and obviously really cool
mechanistically uh medications that
don't pass the bloodb brain barrier but
will work in the periphery to prevent
constipation. But constipation is a big
deal in older patients, younger
patients, too, but it's definitely a big
deal in older patients.
Um, that's for sure. I never realized it
was a medical emergency as much as it
was. Uh, travelers diarrhea. Well, it
says traveler. So, you went somewhere.
All right. Don't make it weird. Um, so
usually these are people that leave the
country, go to some endemic area, and
they get exposed to sources of, you
know, water and other things. And you
know the people in that area are fine
because their bodies have adjusted and
acclimated but yours hasn't. So you end
up developing these relatively acute
onset abdominal pain, cramping,
diarrhea. Uh sometimes it can cause
nausea because if your bowel is wanting
to get rid of something, there's only
two exits up and down. When both are
going on, it's called gastronitis.
However, if it's bacterial uh in origin,
typically what we see as more just
diarrhea, just just profuse, you know,
diarrhea. So, our whole goal is keeping
control of the symptoms. I mean, it's
nothing wrong with having diarrhea as
long as you're not having fluids and
electrolyte abnormalities. So, oral
rehydration is really key. Uh if it is
uh since travelitis seems to be
associated with um organisms u classic
agents are probably zipro rafaxamin
being the two most common. Um if you
have some sort of allergies that may be
a zithroyiain.
There's a little bit of debate about the
use of antidiaral agents simply due to
the fact that if you think about your
body wanting to try to get rid of
something that ain't supposed to be
there you shouldn't clog you know reduce
its ability to do that. At the same
time, you don't want to have the other
extreme of uh fluid and electrolyte. So,
there's a lot of debate, but from a a
evidence-based standpoint, there's no
evidence that using lyramide
intermittently, even for some
symptomatic control is detrimental to
the patient. Now, if someone has toxic
megaolon and they have inflammatory
bowel disease, something else that's
going on, that's totally different.
Gird, uh, I think I have reflux right
now. Uh, I'm just kidding. Um, but
reflux is caused by a number of things
too, right? It's basically acid spending
too much time in the wrong place.
Supposed to be in the stomach. We get a
little bit of reflux that comes up
through the lower esophageal sphincter
every once in a while and our normal
saliva and just gravity and parasic
movements wash it off. Uh, but if it
stays there for too long and it spends
too much time there, then it starts to
irritate the tissue and that's where
people start to get pain with
swallowing. They can develop
strictctures. Uh when they lie flat,
they start to get aspirations. They can
taste uh and perceive a metallic sort of
sour sensation in the in the back of
their throat. Okay. So, how do we do
that? Well, one is prevent the esophagus
from letting too much acid come up. So,
it could be anatomical, right? Hyal
hernas, that's a surgical fix, not a
pharmacologic, but there could be drug
induced. So anything that relaxes smooth
muscle or skeletal muscle at any sort
level uh like calcium channel blockers
have the ability to relax lower
esophageal sphincter and cause too much
acid to spend too much time up in the
esophagus. Nitrates can also relax it.
That's why we use it for nutcracker
esophagus or esophageal spasms because
it can relax the smooth muscle of the
esophagus. Caffeine uh you know I'm
going to get a little swig of that.
Theophelin those are classic
bisphosphinates don't necessarily cause
gird but obviously they can exacerbate
lower esophageal irritation especially
if they don't get all the way down into
the stomach from inadequate uh oral
hydration. So what do we do? Have the
patient sit upright. Uh try not to wear
clothes that don't fit you right too
tight. Uh putting on the belt too tight
because you're sucking everything in.
Well, it's just pushing everything up.
Uh the other patient population that has
that problem are pregnant patients. Um
so those who have something in their
abdomen pushing their stomach up uh
struggle with this all the time. Uh uh
so you know just think about those
things that are just uh normal. Uh H2
receptor antagonists are helpful for
mild to moderate conditions. Obvious you
will overdevelop some tolerance over
time because there are other mechanisms
and pathways to which you make acid. So
if you have a little bit more severe
chronic problems and you are not getting
the relief from H2 receptor antagonist
use after several weeks then you
probably should consider a PPI that
doesn't result in a tolerance
development. Why are we doing this?
Well, we want to make sure the patients
don't develop Barrett's esophagus which
is basically a transition of the cells
at the lower esophageal area to a uh
pattern that looks like it is in the
stomach. And basically that's called
Barrett's esophagus. Um, and people can
develop early esophageal cancer. By the
way, gavascon,
over-the-counter gavascon, uh, which is
a kind of like an oral antacid, has um a
algenic acid in it. It's one of the only
formulations that it coats the esophagus
and creates a little bit of a barrier.
So, it's a really good more expensive
oral ant acid that you can um sometimes
use. Uh, Dr. in anything so far that you
want to throw in or are we just going to
keep we keep going?
>> Just maybe a clinical pearl might even
be something that you would actually see
on the exam, but the PPIs are a lot like
insaids in the sense that uh you can
need more than a one trial of one agent
to find something that's effective. So
just because a merazole doesn't work uh
doesn't mean you shouldn't try another
one in the same class. Kind of like
insaids. If ibuprofen doesn't work, you
might try neproxin. So um Absolutely.
Clinically think about that.
>> Yep. There are genetic polymorphisms
that influence the activation of some of
these drugs that may influence the
efficacy that Dr. Bolan is talking
about. Also, don't forget there are
drugs that require acidic environment
for adequate absorption and
bioavailability. That's your adanir
which is your protease inhibitor for the
treatment of HIV in uh itchonazol
capsules. uh you've got some of the uh
tyrroscen kinace inhibitors like arotnib
to satin those agents are classically
needing uh adequate amounts of acid to
be absorbed. Hemocchromattosis too much
iron your body is not getting rid of it.
Uh sometimes you can get that from
getting too many blood transfusions and
we see that in patients like with cickle
cell disease or women who have
significant um uh menstrual cycles and
find themselves getting repeated uh
transfusions and ultimately probably
have fibroids and need to have a
unfortunately a hysterctomy in those
situations. Uh but you can accumulate
too much iron. um most of the time when
we think about hemocchromattosis we're
think about the hereditary type where
you essentially uh can't get rid of it
um and so it's you know that accumulates
in your body deposits in various organs
your joints the one area organ that we
most get concerned about is the liver in
particular which can then cause liver
damage so the way you get rid of it is
well get rid of the blood so you can do
phbotomy which you know is somewhat
invasive and problematic uh until you
get some of the iron levels down.
The other thing is you'd give bile or
binding agents. Chelating agent like
dufferoxamine in particular is probably
the most common. All right, moving on to
inflammatory bowel disease. Crohn's and
ulcerative colitis. So Crohn's is one of
them, but Crohn's is different than
ulcerative colitis in that it is
intermittent throughout from the oral
fernx all the way down to the rectum.
Most common location is the terminal
illium. Okay. And these patients can
have abdominal pains, cramps, so we call
it bilary collic. They will have
diarrhea. Although the diarrhea in
Crohn's tends to be less bloody than
compared to ulcerative colitis. Uh
Crohn's patients can also develop these
fistulas which are basically little
holes or conduits between organ tissues.
I've actually seen uh someone develop a
fistula to their back. And so literally
they have stool draining out of their
back. Uh I mean it's crazy what happens
with this disease. Um when you do a uh
colonoscopy or a pill endoscopy, you
basically see these skip lesions that
don't follow the pattern of all sort of
colitis. Um and then you could obviously
get tissue uh samples. Now there's mild
to moderate disease and then there's
more severe and recurrent. mild moderate
you're looking at initially since we
don't want to go the invasive route five
ASA products which are amino
salicellates which strategically are
formulated to uh release their chemicals
in the ASA product at different phes in
the body they tend to work a little bit
better uh in all sort of colitis because
of their uh activation predominantly in
the large intestine um you have
antid-diarral agents intermittently uh
steroids because the inflammatory
response or the immune systems or
activation and then antibiotics
antibiotics especially if you have
fistulas and then lastly demarss in
particular the uh TNF alpha antagonist
so infleximab adalumab or tannercept
these drugs have also gained a lot of uh
use in this disease uh because we
ultimately want to try to prevent some
of the surgical fixes which would
include resection of the bowel and in
this case uh be the terminal ilium which
is where B12 then gets absorbed causing
B12 deficiency in these patients. Very
classic. So you can have bowel
resections and use of biologic agents.
Moving on to ulcerative colitis. It is
restricted to the colon. Uh it starts at
the rectum. Remember it moves backwards.
So in a proximal format. So you do a
colonoscopy and you see how far up it
goes because that determines also what
dosage formulations you can use. So we
have suppositories, we have foams, we
have enemas and the enema can make it
all the way up to the splenic flexure
whereas a suppository is only going to
go you know maybe uh 10 10 cm maybe u
especially if you lay on your left side
but these patients tend to have a lot
more bloody stools and can develop toxic
mega colon where their bowel basically
gets really large gets so large and
because of its frailty can perforate and
basically pop open. Uh that's bad. You
don't want that to happen because then
stool leaks out in the paritinium and
that is a life-threatening medical
emergency. So five ASA products tend to
work a little bit better in ulcerative
colitis because of their localized
effect in the area where they get activated.
activated.
Uh you also have your demarss your TNF
alpha uh and inhibitors including plus
or minus steroids. Um, if you're having
an acute flare and there's any evidence
or concern of toxic megolon, hands down,
do not give anything that slows down the
bowel paristalsis. Okay? No opioids, no
anticolinergics, no loperamide, none of
that stuff because if it you accumulate
more air and it perfs the bow, you've
got yourself a problem. Now, if this
becomes recurrent and they just can't
get better despite steroids and all this
stuff, you can remove the colon and put
in a colostomy for a period of time. let
things calm down, wean them off the
medications, get them off the steroids
that they've been on, and then you can
reconnect the bowel and create what is
called a J pouch where they basically
have retrain themselves and teach
themselves how to hold on to stool
before they uh defecate. Um
so, uh irritital bowel syndrome, uh Dr.
Bolan, anything there for inflammatory bowel?
bowel?
No, just maybe thinking about, you know,
if you're looking at a case or a
patient, you know, make sure you check
their allergies, you know, in case they
have a sulfa allergy or something like
that. Just pay attention to
>> Yep. sulfa salazine for sure. If you end
up going that route with a 5A product
that has that. Absolutely. And then also
don't forget with TF alpha antagonist,
you've got to screen and ask for whether
or not they have any risk factors for TB
and rule out latent TB before you ever
give anybody a TNF alpha antagonist. And
also don't use TNF alpha antagonist in
patients with class three or four heart
failure. All right. IBS
basically irrital bowel. Basically what
it is it the bowel is irrit irritated
and it will have these spasms and cramps
and people get gicolic and bloating.
Again they will have uh two different
types. There's IBS with predominant two
main types. There's miscellaneous and
mixed and all that crap no pun intended
there. uh but there's IBS predominant
constipation and IBS predominant
diarrhea and as I said some people can
have a mix and miscellaneous um so the
Rome four criteria kind of are what are
standard many times you will see uh
concominant or um patients have
psychiatric illnesses uh depression OCD
anxiety disorders based on when you look
at some of the epidemiologic data on
these patients so depending on what type
of problem you're
governs which type of drugs you use. So,
there's been some evolution in this area
for a while. Some of these drugs are
also used for idiopathic chronic d uh
constipation. I didn't make a lot of
mention of them because they're
typically not firstline agents. They're
not either in this section here. Uh but
you can see we have some of the guanace
agonists and then we have the chloride
uh channel activators. Uh laparroone in
particular has been around for a little
while. Um if you have the diarrhea
predominant the one thing that I would
mention is elocatron is one that can
cause es schemic colitis. Um so you do
want to be careful with that particular
um agent in IBS.
Uh but IBS is almost sometimes also if
you look at the Rome criteria it's
almost a diagnosis of exclusion which
means you've got to rule out other
things. Um and again try to treat the
underlying psychiatric condition if it
is there because the psychometric part
of it is seems to be a big contributor.
All right moving on to a couple of the
complications in cerosis or liver
disease. So the liver break you know
obviously can't uh do some of its
activity. So some of its synthetic
function is compromised in particular
with ascites we don't have enough
albammen. Um and we also have
endothelial dysfunction which causes a
redistribution of blood volume and it
changes the enotic pressures within the
vascular space. And when you create that
pattern with increased hydrostatic
pressures with low encodic um pressures
then you push or encourage fluid to
escape the vascular space out into the
peritineal environment. Right? So they
get abdominal distension.
Usually they're not painful and where
the pain comes in is usually from it
being tight asites where they look like
they have you know quadruplets in their
abdomen, right? Um, and so they usually
have a positive fluid wave. You can do
an ultrasound and clearly see this and
it's pretty straightforward. When you do
a diagnostic parasentesis and you send
that off to the lab, you're looking for
evidence of infection, which incites
only, no SBP, the neutrfil count is less
than 250. Their sag is greater than 1.1.
So that's the serum albammen acidic
gradient. So you need albammen
concentrations between the two. So how
do we treat it? Well, for the most part,
you water and salt restrict them um so
that they hold on and try to pull that
fluid back out. If they're really tense
and having shortness of breath or
discomfort, you can do a therapeutic
parentesis, which is essentially just
drain it all off and then start them
back on some diuretic therapy. Diuretic
therapy being high dose bonolactone at a
ratio with some ferosomide to get rid of
some of the potassium that happens with
these doses. But you're looking at big
doses 100 100 milligrams of aspirone for
uh and and 40 milligrams of uh feros
ferosomide and you can do that push that
all the way up to 400 u but you risk of
hypercalemia from that which is why the
lasex is being given but you want to be
careful not to give too much lasix
because you can put the patient into
hpatrenal syndrome esophageal veraces.
So, just like I was saying, when you
have this increased hydro or this
pressure that's pushing on these walls,
they start these vessels or veins start
to dilate and they're weak weaker
um uh blood vessels and so they can pop.
Okay? Well, why does that matter? Well,
because remember the synthetic function
of the liver is also compromised. Well,
the liver also makes clotting factors.
So, if you're not making clotting
factors, then you can't stop yourself
from bleeding. And then that's when
these patients start having you know hematis
hematis
and if it's profuse then they can bleed
to death essentially. So this is a
life-threatening medical emergency which
requires uh urgent or an emergent um uh
endoscopy where they ban the esophageal
veraces or they do sclerotherapy.
Um if you're putting Blakemore tubes in
the patient's probably going to die. Um
so that's just I mean that's the tube
that you basically put in there. balloon
onto the esophagus and you wear the
football helmet and all that stuff. I
mean, you're in that situation. Um,
that's not a good scenario. Um, so
endoscopic intervention is the is this
classic treatment. Um, PPIs aren't
really going to do a whole lot other
than what you're trying to do is raise
the pH greater than six so that you can
maximize coagulation. Octriotide um has
been shown to redistribute blood flow
throughout the splanknic circulation. So
where all this pressure is, it can
tighten down on those vessels a little
bit. And then don't forget any
esophageal veraces that bleed, you need
sept trioxone to prevent SVP. Star it,
remember it, sleep on it, go in the test
knowing that. Uh it sounds counterintuitive
counterintuitive
uh but it is a huge intervention that
has been uh shown to improve uh many
outcomes in serotic patients.
The other is synthetic function of the
liver is to metabolize things and
there's a lot of things waste products
that it gets rid of so that we can
eliminate it in the urine but one of
them are these nitrogenous substances
and particularly ammonia which can pass
through this uh bloodb brain barrier and
cause altered mental status. So um but
just keep in mind that altered mental
status does or high and sephilopathy
doesn't require elevated ammonia levels
but most of the time you see it. So you
always always want to think what else
could be causing this infection.
Infection and infection in a serotic
it's set BP until proven otherwise GI
bleed. Second, why GI bleed? Well, blood
is leaking into your stomach. And guess
what you do? Just like when you eat
steak, you digest the blood in the meat.
It's red meat for a reason. So when you
digest blood, you're digesting
hemoglobin, which is proteins, which the
end product of that is ammonia, right?
So you can't get rid of these things and
you accumulate it. So one of the ways
you get rid of it is to ex increase the
excretion through the GI tract. So we
give lactulose if they're not altered
mentally. You give it orally till they
develop loose stools. Two to three loose
stools per day. Not watery diarrhea.
More is not better. It's not the
American way here. Okay? It's not a big
size it anything like that. It is two to
three loose stools because if you cause
diarrhea, the fluid that's causing the
get that you create diarrhea from is
coming from the vascular space can throw
them into syndrome. If they're confused,
altered and you can't use their oral
airway uh oral fairings to ingest it
without aspirating, then you use the
other opening.
Nurses do not like you when you put the
orders in or make the recommendation for
rectal administration of lactulose
because it's a big mess. How do I know
that? Because I was a nurse before and I
was the had to take care of patients who
got rectal laculos. Ain't fun. Okay. Uh
but it's the right thing to do for the
patient. Um hippatenal syndrome I've
mentioned a couple times. There's two
types basically. Type one is the rapid
decline of kidney function. So an acute
kidney injury essentially. Type two is a
slow gradual decline. Most patients with
type one when they start to develop it
die within a week. Okay? They don't it's
not a abrupt sudden death within the
next hour. It's usually over a couple days.
days.
Um there's not a whole lot you can do
for this situation. Uh there are some
drugs like vasop prein madrin octriotide
that have been studied. uh some patients
if they qualify for tips and you have
the appropriate resources to do that
type of procedure maybe uh but it's
difficult uh once these patients head
down that road. All right. Uh Dr.
Boland, anything else? Anything on this
before I jump in SP?
>> Nope, I'm good.
>> All right, SP. Now you got abdominal
pain and you've got a fever. So in a
case that's the big thing that's going
to differentiate ascites from SP.
They're going to have a fever. You're
going to tap them. You're going to get
the fluid off. It's going to be cloudy,
right? And you're going to get PMN's
back that are over 250. That's your
classic pattern. So, septraxone or
sephottoaxine. Actually, if you're an
evidence-based purist, you're going to
go with sephotaxine. But septraone is
the most common thing thing available in
clinical practice and that's what most
people use. Here's the key, guys. Make
sure you add the albamin on on day one
and day three. Do it. That's a that's a
common missed area on this portion of
the exam. So whether you're taking BCIDP
or you're taking um you know BCPS or you
know BCCCP CCCP
CCCP
I don't know I just made that one up but
you know there's so many BBC's
whatever that it get confusing but
acutely you got to treat it with one of
those antibiotics plus the albamin. If
you're doing prophylaxis then afterwards
you cypro or noroxicin are the most
common although I don't quite honestly
have never seen noroxisin uh but
theoretically you can get it all right
canabonoid hypermesis syndrome it's too
much of this right um so don't do that
okay that's how you treat it stop right
I mean I can't tell you I I when I
trained at Hopkins in Baltimore these
guys came in every shift like it was no
one's business and here we are pushing
you know marijuana across the country
anyway whatever uh what do I know um but
they come in and they have like profuse
severe uncontrollable
vomiting and it is just this constant
and they are miserable. So some of the
things that they will a lot of times try
are hot showers uh but really you have
to just stop them from taking and
smoking the marijuana. Um but in the
acute situation what you can kind of do
is calm them down and sedate them
essentially. So that's where dyen
hydramine is helpful. Dyen hydramine has
anti-imetic properties. Dropodol has
anti-imetic properties and
antihistaminic properties. Um capsation
cream has actually been associated
with benefit outcomes and you basically
rub it all over their abdomen and get
their abdomen to burn.
That sounds like fun. Oh, you're
vomiting. Hey, by the way, I'm gonna
make your abdomen catch on fire.
You're gonna do what? Right. But why
would we do that? So, remember when you
uh blah
then the name of the receptor just went
anyway, uh there are some receptors nerves
nerves
on that one.
>> Anyway, anyway, it will come to me. I
promise. Uh but at any rate, when you
activate these receptors, they
basically, you know, create pathways
into the central nervous system that,
you know, suppress other pathways. And
so the idea is that it creates sort of a
a negative feedback on another pathway.
Um so you cause pain and you get another
effect kind of like you know why we use
capsation at some level anyway. Um oh
that's driving me crazy.
All right. Anyway, uh nausea, vomiting
with pregnancy. So during pregnancy uh
estrogen, progesterone levels go way up.
So does beta hcg. And those things are
what trigger uh a lot of the uh early
phases of um morning sickness. At some
level, it's actually a sign of a healthy
pregnancy because I mean the hormone
levels are high. Your hCG is high. Uh
it's miserable uh for the patient
obviously. Um and it can get to be
significant where there's volume
depletion and electrolyte abnormalities
if they can't keep anything down. So
you're not just trying to hydrate uh the
the mom, but you're hydrating a placenta
that needs to be perfused. So if you
remember, your plasma volume during
pregnancy goes way up. All right?
Because you've got to profuse another
organ and another patient. So like
there's a lot going on there. So this is
where in the acute you know many times
these patients have to come in they get
IV hydration and then we give them some
anti-imetic therapy recognizing that in
the first trimester which is in the
first you know 10 to 12 weeks here
you're getting where organogenesis and
differentiation is occurring. We try to
minimize drug exposure once you get
things to calm down. One of the
preventive agents that you can use is
the doc doxyamine uh with uh purodoxine.
You can buy use the formulation where
it's made that way or you can separate
them out. It doesn't really uh matter.
Of course, the drug company wouldn't
want you to hear you say that.
All right, Dr. Bolan, anything there?
No, I just think it's interesting that I
actually have not seen that used as much
as even nondancetron and the
promethazine which
just a clinical thing just something
I've seen more.
>> Yeah, guys, just so you guys know, a lot
of you threw the answer substance P that
is the old school teaching that is so
wrong. Sorry, I don't mean to be mean.
It's the vanilloid receptor and a
vanilloid one receptor agonist is what
capsation is. Uh so uh it finally came
to me. Thank you guys for a couple of
you throwing the word vanilloid in that
triggered it right away. I snapped out
of my TIA because TIA remember is not
permanent neurologic damage. It comes
back resolution of symptoms. So back at
my baseline here. Uh but uh but just so
you guys know it has nothing to do with
substance P. That's an old school uh teaching.
teaching.
If you see that on a answer as an answer
choice on the test, it's flat out wrong.
All right. Acute pancreatitis. Uh well,
it's inflammation of the pancreas. But
why? All right. So, the pancreas is
digesting itself for some reason.
Pancreatic enzymes got activated. Where
are pancreatic enzymes supposed to be?
In the small intestine. When you eat
food, it secretes it down into the
common, you know, into the common bile
duct and gets into emerges with where
bile is and it makes it goes to the
ampular vader at the sphincter of odi
into the small intestine to digest food.
Well, if something blocks that tube like
a stone from your gallbladder, well,
that can do it. Okay. Uh other common
ideologies is, you know, triglycerides.
Anytime it gets over 500, the risk
starts going up. Definitely goes over a
thousand. The other is drinking.
A lot of drinking, binge drinking most
commonly is where I see it. Patients uh
you know uh go to the beach and uh
spring breaks and things like that and
just drink, drink, drink, drink and then
they have you know this left upper
quadrant pain that radiates to their
back uh uncontrollable nausea and
vomiting. uh if it's bad enough it can
cause hemorrhage and that's the colon
sign and turner signs where blood is
basically leaking into uh the
retroparitinal space and gets to your
back and other things. If you see that
you're in trouble or that patient's in
trouble uh that means that they can
hemorrhage. Why? Because the blood
vessels coming to the pancreas come
right off of the aorta. Bad news. Uh so
that's why we treat it aggressively. We
try to get to calm down. Try to get rid
of the underlying cause. Um, and so the
acute is shut down the GI tract. Don't
do anything to stimulate. NO, NO, NO, IV
fluids. You can give analesics. There is
a historical concern that opioids will
cause spasm of the sphincter of OD. Uh,
that is true. It can happen. Uh, but
it's rare. Okay. Uh, and then obviously
antiimetics. If you have a stone or
something blocking the tube, you might
need ERCP, which is a invasive procedure
to basically put a tube in there or
dilate or extract out the stone that's
blocking uh the drainage of that area.
Okay. Uh chronically, if they keep
digesting their pancreas, then their
pancreas is going to lose its function.
And then these patients may need
pancreatic enzyme replacement so that
they can digest food. How do you know
who needs that? Well, their stools look
weird. They're white, floating, they're
losing weight. that can't absorb
nutrients. That's how you know. So then
you have to titrate the pancreatic
enzymes to meet the needs and not use
too much and then replace their vitamins
because again of nutritional
deficiencies. Peptic
>> also must add just to add in there with
uh pancreatitis you can have drug
induced. So
>> oh yeah don't forget
>> that you know DP DPP4s and GLP1s are
probably the ones that most commonly
come to mind. But if you actually look
into that there are a lot not that
there's a high um high rate of drug
induced pancreatitis with some of the
these other agents but it can be you
know with uh your anti-retroviral
therapy with uh even your oral
contraceptives valproic acid. Um so
there are quite a few drugs that have
you know caused this to some extent.
>> Absolutely excellent point. Peptic ulcer
disease. So you basically have a ulcer
or erosion of the mucosa in the stomach
or in the first part of the deadum. You
don't want a deadinal ulcer. Those can
be life-threatening because it's again
close to a blood vessel right by the
aorta and those are the patients that
have life-threatening GI bleeds. But the
biggest thing here when you have an
ulcer um outside of having dark stools
because the blood finally digests and
makes your stool look black and tar is
that you want to evaluate for the
presence of H pylori. H pylori uh if
it's not considered or treated can cause
recurrent peptic ulcer disease. Um and
so you think about treatment you want H
pi you want phes above four that's what
facilitates healing and so the greater
time of the asterric acid pH above four
that you can get uh the greater the
amount of healing and that's why most
people end up going to PPI because H2
receptor antagonist just don't usually
do that. If you have active bleeding
ulcers like I said in the g or
esophageal veraces lecture that the
reason people use PPIs and highdose PPI
is to maximize the pH above six because
that's where you can in facilitate
coagulation. So in the acute phase
giving a bolus dose of that maybe even
sometimes an infusion may be necessary
but don't forget your H pylori and H
kidneys acute kidney injury AKI
remember it can be prenal before the
kidney like hypo profusion dehydration
right can be intrarrenal something
happened to the kidney you're insulting
it all right infar something's going on
and then it can be postrenal like your
prostate's blocking it or some patient
pulled the foley catheter with a bulb
seen a patient do that before
um so how do we know um you need ur
analysis do you need to memorize this
for board exams probably not I think
they're going to probably give you more
of the diagnosis but when you look at
benocratin ratios and you look at the
fraction of sodium excretion that kind
of puts it into the categories. Okay, so
I'm just going to leave it at that.
There are different stages um of AKI
depending on the degree of kidney change
from baseline um that you're seeing. So
what do you want to do? Well, you want
to consider dialysis if the AKI is
severe enough to where you have a
having you got an acidosis or metabolic
acid base disturbances. E you have
electrolyte abnormalities most commonly
um hypercalemia
with EKG changes significant enough to
warrant that. Uh ingestions that you
need to get rid of these agents like
some of your toxic alcohols and aspirin.
uh and then fluid overload from usually
heart failure and then uremia that is
causing bleeding uh uremic platelet
dysfunction. Um so treat the underlying
cause and get rid of those offending
agents. Don't forget about classic drugs
like NSAIDs, amoglycosides, venkcomy,
cysplatin those being some of your
classic obviously there's a lot of other
ones CKD chronic. Now they start
developing problems because remember our
kidneys normally make arythropoetin
which help us to formulate you know uh
uh red blood cells. So
just like with AKI there are staging of
CKD based on the GFR. Um and so these
patients can develop you know you know
inability to urinate they get fluid
overload they can come in with shortness
of breath heart failure edema anarcha
all electroly abnormalities again
acidbased disturbances. So it just
depends on if it's acute or chronic and
where they're at. Uh so again treating a
AEIOU with diialysis if it's present is
always the right answer and sometimes
patients need acute diialysis to get
things under control. Treat coorbidities
because they are at higher risk
sometimes depending on which guideline
or uh position statement you read from
an organization. CKD be can be
considered more like almost like
diabetes a little bit of that higher
cardio uh cardiovascular risk profile
and then ESAs ariththropoan
stimulating agents um if you're going to
use those remember we don't use those
until the hemoglobin falls less than 10
and if we use them we need to re make
sure that the iron stores are present
and sometimes just giving back iron
replacement solves the problem for CKD
patients and there especially on
diialysis, just give it to them at each
session, 100 milligrams, and you'll
you'll replace it much quicker than you
can do by mouth. Um, but then you can
consider like arythropon um agents um
once the iron is restored, but you don't
want to raise the hemoglobin above 11
because that's where the outcomes go
bad. Anything any on AKI, CKD?
Not the only thing I would say on CKD is
don't forget that you have at least one
you have depaglozen now one of the SGLT2
inhibitors that's indicated whether the
patient has diabetes or not uh to
prevent that progression of renal
disease but be sure you're checking uh
GFR I mean they it goes down quite low
but it's different for different agents
uh and then if the patient does have
diabetes you also have canagal and if
they have albinura so those two can be
added to treatment. One just with
diabetes and one uh can be with or without.
without.
>> Love it. It's awesome. Hypercalcemia.
I'm talking symptomatic. So that's the
bones, groans, stones, thrones,
psychiatric overtones. So that people
talk about classic presentation because
they have bone pain. They have abdominal
pain from the hypercalcemia because the
calcium is used for actyin and it's
contracting the bowel. They're
developing kidney stones. They're on the
ba they're going to the bathroom a lot
because just like with sodium, they
water follows calcium in the urine. So
they pee a lot and then it starts
messing with their brain. So their
calcium levels are over 10.5. Treatment
slam dunk. Give lots and lots of IV
fluids. That's the answer. Not Lasix, IV
fluids. The only reason you ever add on
Lasix is to get rid of the extra fluid,
especially if somebody can't get rid of
it themselves. Okay? But it's really IV
fluids, IV fluids, IV fluids. If after
several, you know, you give them certain
amount of IV fluids, like a liter, two
liters, depending on their size and
their risks and they're still elevated
and they're still symptomatic, then you
can consider a single dose of parental,
okay, not nasal, parental, uh,
calcetonin. You don't want to keep using
calcetonin, you develop calcifilaxis
from it. If your hypercalcemia is
secondary to um malignancy, so you have
a hypercalcemia related to cancer. Okay,
so you have an osteolytic lesions in the
bone essentially. Then you're thinking
of your bisphosinates and it's the
parental bisphosinates. That's your
pomeigronate which is not indicated for osteoporosis.
osteoporosis.
And then zolandronic acid which is
originally came out for hypercalmia
malignancy but then was added as a
single once a year infusion for osteoporosis.
osteoporosis.
But those two drugs are the ones. It's
single dose and remember it takes about
a full week uh for that level to come
down. So it's that's this traditional
sort of pattern that you go through in
treating those patients. What about the
other extreme? Now it's too low. Uh well
this could be for a number of reasons.
It could be from nutritional
deficiencies, poor absorption. It could
be from also uh uh drug induced. It can
also be from h uh low vitamin D levels,
especially in people that live in
certain regions or of the country where
it's uh colder and darker and uh
overcast and they don't get as much
sunlight, those kind of things. So,
these patients can develop muscle
cramps, even spasms. Uh they can develop
seizures. They can develop bronco spasms
from um basically the airways spasming.
uh and then uh increased sort of
reflexes that are a little bit more
hyperrelexic. So their calcium levels
are less than 8.8, you should always
check a vitamin D level because you can
give all the calcium you want, but if
the vitamin D level isn't there, it's
not going to help maintain homeostasis
from other sources. So if you're
symptomatic, IV calcium replacement. If
you have only a peripheral IV, it is
calcium gluconate. If you have a larger
central access point like a central line
or pick line or a IO then you can use
calcium chloride. The difference between
the two is that calcium chloride has
three times the amount of elemental
calcium and is more costic and
irritating to the blood vessels. Um and
so we rather use that when we have a
central line um access
point. Um, the only time that's not the
case is in cardiac arrest. Um, so if
you're in PA arrest, uh, use calcium
chloride in a peripheral IV all day long
because they're going to die if you
don't do something. Um, you don't care
about thrombophilabitis.
Uh, so once you've gotten them out of
that, then it's oral calcium. Just
recognize that your body can only pretty
much maximally absorb 600 milligrams at
any one time, which is why most people
take 600 milligrams in the morning and
at 600 milligrams at night because
that's all you can absorb. The rest of
it's just going to cause constipation.
If you are deficient in vitamin D, most
people would recommend calcatrial, which
is the active form of vitamin D. All
right, moving on to other electrolyte
abnormalities. hypercalemia they'll
probably be in the going back to CKD one
of the most classic electrolyte
abnormalities that people find uh they
just come in with vague symptoms uh feel
bad weak tired they can start having
palpitations if they start having PVCs
all right and that's what we get
concerned about with hypercalemia is
that they start having ventricular
disturbances uh and just so you know
that's part of the cocktail for the
death penalty um you just give an
injection after you give the
penttoarbital and in the sleep, you just
whap them with a big dose of potassium
and that's the end of that. Uh, so too
much potassium is bad. So EKG classic
findings peaked T- waves. They're very
pointy, but I've seen all kinds of EKG
changes, but that's classic, which you
probably see on a board exam. You can
give IV fluids that don't contain
potassium, so just plain old normal
saline, um, and try to dilute it
quickly. But remember, potassium
normally resides inside the cell. You
have to figure out why it was there and
all this thing. If you're having EKG
changes, you want to um kind of
stabilize the cardiac membrane before
you start driving the potassium back in
the cell. Well, what's going to drive
the potassium back in the cell? That's
your insulin, that's your albuterol,
sodium bicarb. Those are the three main
drugs that will turn on the ATP pump and
push it back in. So, when you do that,
you change electrogative potentials and
you could cause irritability. So if you
have ongoing EKG changes, you give the
calcium, gluconate or chloride first,
then you give the insulin with dextrose
and you're giving the dextrose to combat
the hypoglycemia from the insulin. Uh if
that doesn't work or if you have brada
cardia for some reason, give the
albuterol and it's 20 milligrams. So
it's a little bit bigger of a dose.
ultimately these patients probably are
going to need hemodialysis because
you're not doing anything with insulin
and um but aluterol you're just shifting
where it's at. So if their total body
potassium is still too high the only way
you're going to fix that is hemmoiolysis
and that is an indication for hemmoilis.
Uh some people will say oh use kxalate
stuff's awesome. No it's not. It
actually sucks really bad. uh it can
cause eskeemic colitis and paralytic
illnesses. Do not use it. Most people
don't recommend it. Very rarely do we
use it in clinical practice and the
nephologists get really ticked off uh by
it because it starts causing diarrhea
when they're now finally in the
diialysis unit. So the only way to fix
this acutely and quickly the right way
is to essentially uh take them to
dialysis. Not having enough uh potassium
means now that you need to replace it.
Well, there's a couple key issues with
replacement. First and foremost, make
darn sure your magnesium level is
elevated. Magnesium is needed as a
co-actor for the transporter to push the
c potassium inside the cell. Period. So,
if you're low on magnesium, replace the
magnesium. Then you can replace the
potassium. As a general rule, 10 mill
equivalents of potassium chloride will
raise the serum potassium by 0.1. So if
I give somebody 40 mil equivalents
orally, I should theoretically see the
level go up by 0.4, right? So you just
kind of figure out how much you're going
to need. So if you're like 1.2 behind,
you're not going to get there with an
oral regimen because if you keep giving
somebody more than 40 milligrams, you're
going to probably start causing GI upset
and they're going to vomit on you. And
if you give it IV, you have to you got
to be careful how much you give. So the
maximum rate of infusion for most
recommendations institution is 10 mill
equivalents at you know is the safest
one. You can go up to 20 mill
equivalents in an hour but they usually
have to be on a cardiac monitor and
being followed by somebody who knows
what the heck they're doing. Um because
again giving somebody too much potassium
too quickly could kill them.
Um hypommagnesmia.
So you have low magnesium levels. This
has actually been shown to happen in
case reports with PPIs. Interestingly,
these patients typically just like
hypocalemia can develop QRS widening or
QT prolongation.
Um, and they look a lot like hypocalcemia.
hypocalcemia.
And the reason they look a lot like hypocalcemia
hypocalcemia
is because calcium is a dvalent cation.
Magnesium is a dvalent cation. And so
they kind of do similar things. So, if
you're going to need to replace it, um
you can use the oral route, but just remember
remember
if you've ever tried mag citrate,
it opens up one of the exits.
So, be careful.
Uh most of the time, you're going to
have to give it printerally so that they
don't develop the diarrhea. Um Dr.
Bolan, anything on calcium, potassium, magnesium?
magnesium? >> Nope.
>> Nope. >> Okay.
>> Okay.
>> All right. Now, what do you do when you
got low sodium?
Well, it depends on what's the problem,
right? So, chronically, these patients
develop just come in, I don't feel
right. I just feel really tired. You got
a real electrolyte abnormalities. You
get back and they're their sodium is
like 110. Like, geeh. Well, that's a
chronic. You don't get to 110 and just
go, eh, I don't feel right. That's
usually what we see with diuretic
therapy. It's particularly thyide
diuretics chronically in older patients.
If it's an acute drop, so you're in the
135 140 window and you go to 120, this
patient could easily look like they're
having a stroke and be seizing. Okay.
Um, so acute shifts are what cause most
of the CNS sudden changes that are
severe like the agitation and the
psychosis and the focal neurologic
deficits and seizures. So in either
direction they're symptomatic, you've
got to correct it. Remember this is
where you don't want to correct it too
fast. So you've got a 24-hour period.
The most common sited recommendation to
error on the side of human error because
we're all humans and make a lot of
mistakes is 8 mil equivalents in a
24-hour period total. Now, if somebody
is seizing, I might give them hypertonic
saline quickly to raise their uh uh
serum sodium level by two two to three
mill equivalents quickly to get them to
stop seizing. But then I subtract that
two to three from the total of eight.
And for the remainder of that 24-hour
period, then that's all I can give. Now,
you will some see some cited resources
that say 12. So, if it comes up on an
exam, it'll probably be in a range. Uh,
but if you see any answer over 12, it's
flat out wrong. If you see anything less
than eight, they're probably saying
you're not doing it enough. So, if
there's something between 8 and 12 and
it's the only answer option, it's
probably the right answer. Uh, because
there's not a 100% agreement in the
literature. The reason that people error
less is because if you lose track of the
change, these patients typically die
from central pontiumis about three to
four days after you've done that. So
they don't die just right away. They die
later. So you probably have discharged
them home and they go home and die and
you don't even know you screwed up. So
it's a very difficult um scenario that
you don't want to ignore. All right.
>> Sorry about that. I'll just add one
thing that just sort of came to me with
the hyponetriia that I don't think we've
touched on a whole lot is don't forget
that drugs can do all of these things.
Um, you know, with hyponetriia, what
came to mind was SSRIs. You can see that
a lot with your elderly patients. Um,
>> but with hypercalemia, hypocalemia,
hypomag, hyperac I mean a lot of
different drugs can do a lot of these
things too. So, you know, pay attention
to that as well.
>> Yeah. The classic drug that causes the
chronic levels of hyponetriia is a
thazide. And remember that where it
works in the distal convoluted tubule,
that's pretty much the last area for
sodium reabsorption. And although you're
inhibiting five to 15% of sodium
reabsorption, it's not a lot. If you
keep leaking out sodium slowly over
time, you can get yourself down to
levels of 110 112 very easily and not be
psychotic, you know, having neurologic
deficits. Um, so excellent point. All
right. So, neproliasis.
So, you got a stone inside the kidney
and it's usually moving. That's when
they show up because it's uh uh causing
people a lot of pain. And uh for for
men, this is when they they start
screaming like babies. Um,
and and I always tell them that they
they need to start coming up with a name
because this is their baby. Um, and this
is the closest thing to child birth that
they're going to get. So, they need to
rub their wife's feet when they get home.
home.
>> And u, no, I'm serious. I'm not This is
very painful. I've never had one, but
I've seen patients clearly in the
emergency department. They come in,
they're extremely uncomfortable. If
anybody's ever had one, it is extremely
painful. Uh, I have a 100% respect for
it. I don't need one to be figure that
out. Um, but
>> what's that?
>> I lost count of mine when I was pregnant.
pregnant.
>> Oh, okay. Jeez, I'm so sorry.
But I still tell the guys I still tell
the guys that and the wives that are
sitting the room always go.
>> Yeah, you tell him. You tell him. So I
always say you just had a boy and or a
girl and
>> anyway calcium oxilate calcium phosphate
are the two most common types of stones.
We tell people to strain their urine and
bring it back so we can analyze it but
those are the two most common. Um some
people with gout or hyperurasemia can
also develop uric acid nephroliasis as
well but usually you have some sort of
history. So that's the other reason why
we check for it so you can treat the
underlying problem. Uh so usually come
in with unilateral flank pain. So it's
in the kidney where the in their flank
and the CV tenderness. Um and then it
usually radiates down into the inguinal
area associated with nausea, vomiting
because the pain is so bad. Uh they'll
see bloody urine or they will see
microscopic hematia on exam. Our biggest
thing when you're doing a workup on
somebody with a kidney stone and the
reason we do a urine analysis and also
check vital signs is to make sure those
stones aren't infected. So, kidney
infections that have a stone, it could
be the stone that's the infectious
uh piece to it, the stone itself. And if
you don't get rid of the stone, the
patient's just going to keep seeding
bacteria back in. Uh so that is where
it's a little bit of a problem.
Sometimes those stones go down into the
urtors and then they get stuck usually
right before they enter the bladder,
which is the UVJ junction.
Um so what we can do are try to things
to expulse the the stone at that point.
They're not great drugs but you will see
them being used. The evidence to support
them is very weak overall uh but it's
better than uh I guess nothing. So we
treat them with analesia antiimetics and
then many times you will see things like
tamsyloin or even some of the calcium
channel blockers like nifetapine or
amloopene to relax the smooth muscle of
that urer to get it to stop spasming and
to allow that stone to pass into the
bladder. Now they still got to get it
out through the urethra but once you get
it into the bladder you at least got it
out of the most common location where
obstruction occurs. If the stone is
over.7 millimeters, then that patient's
gonna have a hard time probably passing
it. Um, so they might need a stent.
Okay. Um, keeping in mind prevention,
hydration, hydration, hydration, things
crystallize when it's not diluted,
right? So crystallization is that um
calcium, things like that can also be
eliminated at higher concentrations with
caffeine. So people who drink teas and
colas and those kind of things can
sometimes have it more. Um and then
drugs, diuretics have been known to
increase uric acid levels in the body
but also increase calcium um or
electrolytes in the urine. You've got
bactrum that can crystallize. You've got
theopheline, topyramate, zonismide that
have been sort of classic drugs uh for
drug induced.
Okay guys, so uh we're going to take a
quick break here and uh we are on
target. Um and so I know that there's
been a couple questions, but we're going
to take a fiveinut DVT prophylaxis break
and decubitous ulcer prevention break.
So we will see you back in five minutes.
All All right. So, there were a couple of quick questions uh that I think um
of quick questions uh that I think um that I think we can quickly uh try to
that I think we can quickly uh try to answer for those of you uh that asked.
answer for those of you uh that asked. Let me jump on those real quick. Um so
Let me jump on those real quick. Um so the new AGA guidelines have taken
the new AGA guidelines have taken natalysismab off their recommendations
natalysismab off their recommendations and uh certulismab is considered so much
and uh certulismab is considered so much lower on the TNF alpha list. Should
lower on the TNF alpha list. Should these new guidelines be the focus now?
these new guidelines be the focus now? Um so first of all those are uh more
Um so first of all those are uh more difficult to treat patients. Um and uh
difficult to treat patients. Um and uh but but where it remember it takes 6 to
but but where it remember it takes 6 to 12 months and it has to be something
12 months and it has to be something that is well accepted before it makes it
that is well accepted before it makes it to a board exam. Um so Jennifer I don't
to a board exam. Um so Jennifer I don't think it's going to be high yield for
think it's going to be high yield for the exam. uh TNF alpha. Jennifer, you
the exam. uh TNF alpha. Jennifer, you also asked a question about if you have
also asked a question about if you have somebody with latent TB and whether or
somebody with latent TB and whether or not you can use TNF alpha antagonist and
not you can use TNF alpha antagonist and once you screen for them, if they have
once you screen for them, if they have latent TB, you just have to start them
latent TB, you just have to start them on two drug antimicrobial uh anti-
on two drug antimicrobial uh anti- microbacterial therapy. Um and then
microbacterial therapy. Um and then after that point, you can start the
after that point, you can start the medication if needed. But they've got to
medication if needed. But they've got to be put on the antimicrobacterial agents
be put on the antimicrobacterial agents first, the two at least two drug
first, the two at least two drug therapy. Does Lorenex still have the REM
therapy. Does Lorenex still have the REM program associated with it? I I know it
program associated with it? I I know it has a definitely a it used to be REM and
has a definitely a it used to be REM and I and I think it still is at some level.
I and I think it still is at some level. Um I'm not 100% sure. Uh but it does
Um I'm not 100% sure. Uh but it does have the eskeemic colitis uh concern and
have the eskeemic colitis uh concern and a blackbox warning as a result of it. Um
a blackbox warning as a result of it. Um is hypercalcemia
is hypercalcemia um indicated
um indicated for dialysis? I believe so, especially
for dialysis? I believe so, especially if they're symptomatic and they're not
if they're symptomatic and they're not responding to other treatments. Uh let's
responding to other treatments. Uh let's see, Jennifer asked another question.
see, Jennifer asked another question. Hyponetriia, uh is the disease state
Hyponetriia, uh is the disease state usually from free water deficit and you
usually from free water deficit and you want to give PO
want to give PO free water?
free water? Um
so no, so it's usually hyponetriia is usually from SIADH most commonly. Um,
usually from SIADH most commonly. Um, and you want to free water or restrict
and you want to free water or restrict them. Um,
them. Um, in that situation,
in that situation, I don't know if I answered that question
I don't know if I answered that question very well, but that's what it is. Uh,
very well, but that's what it is. Uh, can you go over the current treatment
can you go over the current treatment recommendations for H pylori? So, uh,
recommendations for H pylori? So, uh, it's a different Jennifer. Uh, so
it's a different Jennifer. Uh, so there's two 14week or 14-day uh, sorry,
there's two 14week or 14-day uh, sorry, 14-day treatments. There's four drug
14-day treatments. There's four drug therapy, no longer three drug therapy.
therapy, no longer three drug therapy. So, you have your PPI.
So, you have your PPI. uh you have the um Pepto-Bismol based
uh you have the um Pepto-Bismol based therapy with tetracycline and
therapy with tetracycline and metroniditool and then there's the PPI
metroniditool and then there's the PPI non pepto regimen PPI amoxicylin
non pepto regimen PPI amoxicylin uh chloriththomyin and I think
uh chloriththomyin and I think tetracycline or something like that uh
tetracycline or something like that uh but it's 14 days so there's a
but it's 14 days so there's a pepto-based and a non-eptobase
pepto-based and a non-eptobase um
um let's see uh what is the best way to
let's see uh what is the best way to distinguish between prennal and ATN in a
distinguish between prennal and ATN in a uh the urinal analysis. So in ATN you're
uh the urinal analysis. So in ATN you're going to see casts and you're going to
going to see casts and you're going to see um basically damaged particles of
see um basically damaged particles of this of the tissue in acute tubular
this of the tissue in acute tubular necrosis and the casts are probably the
necrosis and the casts are probably the classic finding on a ur analysis that
classic finding on a ur analysis that you'll see or microscopic analysis. Uh
you'll see or microscopic analysis. Uh would would you rather deal with
would would you rather deal with kaillate or p?
All right, Stephen. Um,
Um, oh, hyperonatriia is a freewater deficit
oh, hyperonatriia is a freewater deficit disease. Oh, okay. So, um, so yeah, so
disease. Oh, okay. So, um, so yeah, so there's different types of hyperatriia,
there's different types of hyperatriia, you would need a urine analysis
you would need a urine analysis um in a fina to kind of help you um to
um in a fina to kind of help you um to to discern, but because you want to make
to discern, but because you want to make sure that that what type of you can have
sure that that what type of you can have fluid overload, hyperatriia as well. So,
fluid overload, hyperatriia as well. So, you got to be careful with that. Um and
you got to be careful with that. Um and you see that sometimes with heart
you see that sometimes with heart failure patients. Um so it just depends
failure patients. Um so it just depends on on the situation. But yes, usually
on on the situation. But yes, usually um free water is typically the treatment
um free water is typically the treatment that you go through D5W is an option. Um
that you go through D5W is an option. Um but you have to discern the type of uh
but you have to discern the type of uh hyper treatment that you're dealing
hyper treatment that you're dealing with. So it's not as straightforward. I
with. So it's not as straightforward. I think it's low yield for the board
think it's low yield for the board exams. Okay. I think that was most of
exams. Okay. I think that was most of the questions from session one. So we're
the questions from session one. So we're going to keep going on to session two
going to keep going on to session two because we are doing all right. So we've
because we are doing all right. So we've hitting these good contents. So now
hitting these good contents. So now we're going to get into geriatrics. The
we're going to get into geriatrics. The geriatrics also starts to bridge into
geriatrics also starts to bridge into the neuro uh pieces. So we've got
the neuro uh pieces. So we've got Alzheimer's disease where we have a
Alzheimer's disease where we have a progressive neurodeenerative disease in
progressive neurodeenerative disease in part related to the accumulation of
part related to the accumulation of proteins that shouldn't be there and
proteins that shouldn't be there and they form these neuropibrillary tangles.
they form these neuropibrillary tangles. It results in uh loss of short-term
It results in uh loss of short-term memory. Um these patients then start
memory. Um these patients then start getting confused, have changes in
getting confused, have changes in behavior. Um really the only way to
behavior. Um really the only way to diagnose this is clinically. these other
diagnose this is clinically. these other things that you see on CSF and
things that you see on CSF and histologic uh the the Brack and Rex
histologic uh the the Brack and Rex staging is a hisystologic that means
staging is a hisystologic that means it's postmortem where you did a brain
it's postmortem where you did a brain biopsy don't want to do that um so
biopsy don't want to do that um so that's typically a diagnosis that is
that's typically a diagnosis that is made more definitively after death but
made more definitively after death but acetylonsterase inhibitors are the drugs
acetylonsterase inhibitors are the drugs of choice in this situation because we
of choice in this situation because we don't have anything else that's worth a
don't have anything else that's worth a darn um and so dinepazil owns the market
darn um and so dinepazil owns the market in this group it's easier to dose it's
in this group it's easier to dose it's once a day uh whereas rivistine and
once a day uh whereas rivistine and glantamine require multiple uh
glantamine require multiple uh administrations and are associated with
administrations and are associated with a slightly more GI side effects.
a slightly more GI side effects. Overall, these drugs really don't reduce
Overall, these drugs really don't reduce the progression of this disease because
the progression of this disease because they're not treating the underlying
they're not treating the underlying problem, but they can help reduce the
problem, but they can help reduce the time needed before somebody gets
time needed before somebody gets admitted to basically a nursing home or
admitted to basically a nursing home or something like that. The use of uh NMDA
something like that. The use of uh NMDA receptor antagonists like mamantene is a
receptor antagonists like mamantene is a hit or miss. People tend to reserve it
hit or miss. People tend to reserve it for more moderate to severe disease on
for more moderate to severe disease on top of dinepazil.
top of dinepazil. The reason that this class of drugs has
The reason that this class of drugs has not grown in a disease that is uh a huge
not grown in a disease that is uh a huge cash cow if you could find a drug u is
cash cow if you could find a drug u is that the drugs just don't work. So if a
that the drugs just don't work. So if a drug class isn't proliferating there
drug class isn't proliferating there probably is an efficacy problem. Um so
probably is an efficacy problem. Um so uh Dr. Bolan anything here that you
uh Dr. Bolan anything here that you wanted to add?
wanted to add? No, just, you know, in thinking
No, just, you know, in thinking clinically about this, be sure that
clinically about this, be sure that you're not, even looking at it from a
you're not, even looking at it from a board exam perspective, know when to
board exam perspective, know when to take them away, you know, when they're
take them away, you know, when they're not providing any
not providing any >> therapeutic benefit. Yep. No need to
>> therapeutic benefit. Yep. No need to just keep making them vomit for nothing.
just keep making them vomit for nothing. >> Yeah.
>> Yeah. >> Um, so Parkinson's disease is sort of
>> Um, so Parkinson's disease is sort of the opposite problem. They don't have a
the opposite problem. They don't have a a problem with not enough colonergic.
a problem with not enough colonergic. they have too much colonergic activity
they have too much colonergic activity because they've lost the dopamineergic
because they've lost the dopamineergic input to the sub by the substantia
input to the sub by the substantia and so the overall net effect is an
and so the overall net effect is an overactive colonergic system. So they
overactive colonergic system. So they get these resting tremors bradicynisia
get these resting tremors bradicynisia postural instability. Uh you can do PET
postural instability. Uh you can do PET scans to sometimes help you with the
scans to sometimes help you with the diagnosis but again a lot of it's
diagnosis but again a lot of it's clinical uh drugs of choice usually
clinical uh drugs of choice usually start out for most patients carbodopa
start out for most patients carbodopa leodopa especially if they're older
leodopa especially if they're older patients. If you're even a younger
patients. If you're even a younger patient with early disease onset, then a
patient with early disease onset, then a dopamine antagonist, dopamine agonists
dopamine antagonist, dopamine agonists uh are the drugs that may be reserved
uh are the drugs that may be reserved for that because once you start
for that because once you start carbodopa leodopa again the majority in
carbodopa leodopa again the majority in the historical teaching you got about a
the historical teaching you got about a 5year window. Again, we're not treating
5year window. Again, we're not treating the underlying reason that the
the underlying reason that the dopamineergic cells are dying or going
dopamineergic cells are dying or going away. We're just trying to maximize the
away. We're just trying to maximize the dopamine that is present and provide
dopamine that is present and provide enough precursors to form dopamine in
enough precursors to form dopamine in the central nervous system. So remember
the central nervous system. So remember the leodopa does not pass through the
the leodopa does not pass through the bloodb brain barrier. It facilitates the
bloodb brain barrier. It facilitates the uh I'm sorry the carbodopa does not pass
uh I'm sorry the carbodopa does not pass through the bloodb brain barrier. It
through the bloodb brain barrier. It helps the leodopa get into the blood
helps the leodopa get into the blood brain barrier so they can be converted
brain barrier so they can be converted to dopamine where we want it to work.
to dopamine where we want it to work. Dopamine agonists are what they are.
Dopamine agonists are what they are. They stimulate dopamine receptors and uh
They stimulate dopamine receptors and uh mimic the replacement of dopamine. So
mimic the replacement of dopamine. So they're also not treating the underlying
they're also not treating the underlying problem. Even the catakol methyl
problem. Even the catakol methyl transferase inhibitors uh tacopone and
transferase inhibitors uh tacopone and um tocopone and um and tacopone uh those
um tocopone and um and tacopone uh those two drugs as well as sleene and uh
two drugs as well as sleene and uh recaguline which are your monomine
recaguline which are your monomine oxidase inhibitors they're just
oxidase inhibitors they're just preventing the breakdown. So, we're just
preventing the breakdown. So, we're just adding on those drugs as adjuncts to
adding on those drugs as adjuncts to modulate the symptoms that these
modulate the symptoms that these patients are having to maximize their
patients are having to maximize their quality of life without causing too many
quality of life without causing too many side effects. But anytime you give
side effects. But anytime you give somebody too much dopamine, you can
somebody too much dopamine, you can stimulate problems. So, think about
stimulate problems. So, think about schizophrenia and anti-csychotic
schizophrenia and anti-csychotic therapy. What are we giving?
therapy. What are we giving? Antiscychotics are typically modulating
Antiscychotics are typically modulating the uh an activity of dopamine by
the uh an activity of dopamine by inhibiting it. So if we give somebody
inhibiting it. So if we give somebody dopamine or we increase dopamine or you
dopamine or we increase dopamine or you use crack and cocaine and increase
use crack and cocaine and increase dopamine, you're going to become
dopamine, you're going to become psychotic.
psychotic. So they start having hallucinations,
So they start having hallucinations, delusions, psychosis.
delusions, psychosis. Um and these can be a big problem um in
Um and these can be a big problem um in patients. Behavior changes occur.
patients. Behavior changes occur. There's also issues especially with a
There's also issues especially with a dopamine agonist where they've caused
dopamine agonist where they've caused not only uh uh significant um like
not only uh uh significant um like instantane almost like a rim um sorry
instantane almost like a rim um sorry narcoleptic kind of events where they go
narcoleptic kind of events where they go into these sudden sleep attacks which
into these sudden sleep attacks which can be a problem because they fall or if
can be a problem because they fall or if they're operating machinery which you
they're operating machinery which you would hope they aren't then they can you
would hope they aren't then they can you know hit the ground and hit their head.
know hit the ground and hit their head. Uh but also addictive behaviors. So
Uh but also addictive behaviors. So remember you're stimulating the reward
remember you're stimulating the reward pathway. Um, and so hypersexuality even
pathway. Um, and so hypersexuality even in the older population, addictions that
in the older population, addictions that start getting ramped up like gambling,
start getting ramped up like gambling, people have lost their their homes,
people have lost their their homes, their retirements. I mean, it's a big
their retirements. I mean, it's a big deal. Um, just at a quick little pearl,
deal. Um, just at a quick little pearl, we'll talk about um, uh, restless leg
we'll talk about um, uh, restless leg syndrome a little bit later in the
syndrome a little bit later in the neuros section, but your dopamine
neuros section, but your dopamine agonist and doses that are much less,
agonist and doses that are much less, okay, and basically dosed at bedtime
okay, and basically dosed at bedtime only are used for restless leg. when
only are used for restless leg. when it's dosed for Parkinson's disease,
it's dosed for Parkinson's disease, you're talking about twice a day or
you're talking about twice a day or three times a day uh administration.
three times a day uh administration. Anything on Parkinson's?
>> Um I don't think so. Uh just maybe be sure you're thinking about, you know,
sure you're thinking about, you know, what you would do with on time or
what you would do with on time or wearing off and those types of things.
wearing off and those types of things. You thinking about those from an exam
You thinking about those from an exam perspective.
perspective. >> Yeah. On time and off time. That's where
>> Yeah. On time and off time. That's where your immediate release and your long
your immediate release and your long acting options start coming into play.
acting options start coming into play. um you know how do you adjust those? You
um you know how do you adjust those? You need a basically a journal of their
need a basically a journal of their symptoms to know where the problem is
symptoms to know where the problem is and how you need to make adjustments.
and how you need to make adjustments. But that's an excellent observation.
But that's an excellent observation. Um all right. So BPH
Um all right. So BPH uh that's enlarged prostate usually
uh that's enlarged prostate usually causing outflow obstruction. So they
causing outflow obstruction. So they have difficulty starting their stream
have difficulty starting their stream and then they have difficulty emptying
and then they have difficulty emptying their bladder. So um most of the time
their bladder. So um most of the time the urine flow is low and then they're
the urine flow is low and then they're they have postvoid residual and so the
they have postvoid residual and so the reason that this is a problem is that it
reason that this is a problem is that it also that scenario with retention of
also that scenario with retention of urine increases the risk of UTI. So, in
urine increases the risk of UTI. So, in the male population that as you see them
the male population that as you see them get older, they'll start developing more
get older, they'll start developing more UTI and the risk of prostatitis
UTI and the risk of prostatitis um goes up. Where prostatitis is a issue
um goes up. Where prostatitis is a issue where there's an infection of the
where there's an infection of the prostate in a younger otherwise healthy
prostate in a younger otherwise healthy male, it is probably a sexually
male, it is probably a sexually transmitted disease situation that needs
transmitted disease situation that needs to be considered. So, gorrhea,
to be considered. So, gorrhea, chlamydia, um you know, that kind of
chlamydia, um you know, that kind of scenario. Uh so yes surgical
scenario. Uh so yes surgical interventions are can be tried but
interventions are can be tried but that's obviously invasive that's not
that's obviously invasive that's not first line but uh TURP is the historical
first line but uh TURP is the historical um you know option for that five alpha
um you know option for that five alpha reductase inhibitors your dutasteride
reductase inhibitors your dutasteride finasteride these are uh preventing the
finasteride these are uh preventing the conversion of testosterone to the more
conversion of testosterone to the more potent um androgen five
potent um androgen five dihydrotestosterone
dihydrotestosterone uh which would stimulate growth of that
uh which would stimulate growth of that tissue. Um so you it doesn't work right
tissue. Um so you it doesn't work right away. it takes up to two or three months
away. it takes up to two or three months to kind of kick in. Um so it's not a you
to kind of kick in. Um so it's not a you know quick fix. The alpha 1 antagonist
know quick fix. The alpha 1 antagonist um are better at some of the symptoms in
um are better at some of the symptoms in earlier use. Um but some of the non-
earlier use. Um but some of the non- selective agents like tzisin docasin can
selective agents like tzisin docasin can cause orthostasis in this population
cause orthostasis in this population which could be problematic. Um there is
which could be problematic. Um there is a herbal product that works just like
a herbal product that works just like the five alpha reductase inhibitors.
the five alpha reductase inhibitors. Don't forget that is your saw palmetto.
Don't forget that is your saw palmetto. And then theoretically women uh who are
And then theoretically women uh who are of childbearing age shouldn't u be you
of childbearing age shouldn't u be you know if you're a pharmacist shouldn't be
know if you're a pharmacist shouldn't be dispensing this and touching the pills.
dispensing this and touching the pills. Theoretically uh you could absorb it. Um
Theoretically uh you could absorb it. Um and that might cause a tatogenic effect.
and that might cause a tatogenic effect. Um the concentrations you would absorb
Um the concentrations you would absorb are minuscule. The risk of that is very
are minuscule. The risk of that is very low. There's even uh suggestions that
low. There's even uh suggestions that the ma if spouses uh male spouses who
the ma if spouses uh male spouses who are uh taking this that they have to
are uh taking this that they have to wear condoms so that it even shows up in
wear condoms so that it even shows up in the semen and technically the female can
the semen and technically the female can absorb the semen um if it has it in
absorb the semen um if it has it in there but I mean the risk is low but
there but I mean the risk is low but it's not impossible.
it's not impossible. uh overactive bladder. Um this is where
uh overactive bladder. Um this is where you can have you know different problems
you can have you know different problems with stress incur incontinence uh urge
with stress incur incontinence uh urge incontinence or mixed um you see a lot
incontinence or mixed um you see a lot of uh patients kind of run to the
of uh patients kind of run to the bathroom very quickly um or sometimes
bathroom very quickly um or sometimes even have to wear pads because they
even have to wear pads because they can't hold on to it all the time. Um
can't hold on to it all the time. Um this is where we use the anti-muscarinic
this is where we use the anti-muscarinic agents sometimes with anti-spasmotics
agents sometimes with anti-spasmotics depending if they're having bladder
depending if they're having bladder spasms with it that would be your
spasms with it that would be your oxyutin.
oxyutin. Um but to tolerine um solopenosin those
Um but to tolerine um solopenosin those drugs like that are agents that are um
drugs like that are agents that are um helpful. There are other things like you
helpful. There are other things like you know pelvic wall uh floor muscle
