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Session 5 - Live Rapid Review for BPS Exams

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Core Theme

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

know pelvic wall uh floor muscle strengthening exercises weight loss. Uh

strengthening exercises weight loss. Uh there are different procedures that can

there are different procedures that can um pull up the bladder and different

um pull up the bladder and different things that they can do to kind of

things that they can do to kind of reposition it so that it's not as

reposition it so that it's not as irritable on surrounding tissues. um

irritable on surrounding tissues. um especially if there's any evidence of a

especially if there's any evidence of a little bit of prolapse.

little bit of prolapse. All right. Gout from too much uric acid

All right. Gout from too much uric acid and um most commonly it deposits in

and um most commonly it deposits in areas uh or joints like the uh big toe

areas uh or joints like the uh big toe um and that's the hex um area. So the

um and that's the hex um area. So the reason that that happens and most

reason that that happens and most commonly happens in the early morning

commonly happens in the early morning hours is that you know we lie flat at

hours is that you know we lie flat at night and so over overnight we're not

night and so over overnight we're not dependent. So the fluid leaks back out

dependent. So the fluid leaks back out of our tissues and back into our blood

of our tissues and back into our blood eventually goes to our bladder which is

eventually goes to our bladder which is why when you get up in the morning you

why when you get up in the morning you have to pee because you're getting rid

have to pee because you're getting rid of all the extra fluid that sort of has

of all the extra fluid that sort of has been reabsorbed throughout your body. Um

been reabsorbed throughout your body. Um but when you do that you concentrate

but when you do that you concentrate fluids in every area are areas and so if

fluids in every area are areas and so if you have high uric acid levels they can

you have high uric acid levels they can precipitate no different than kidney

precipitate no different than kidney stones and they can precipitate in the

stones and they can precipitate in the urine and that's where they get uric

urine and that's where they get uric acid nephrolithasis. So it can

acid nephrolithasis. So it can crystallize anywhere. So the big toe it

crystallize anywhere. So the big toe it can go into the ankle the knee the elbow

can go into the ankle the knee the elbow seen it in the wrist. So, um, basically

seen it in the wrist. So, um, basically it's significant redness, swelling,

it's significant redness, swelling, extreme amounts of pain, uh, from this.

extreme amounts of pain, uh, from this. And so, the only true way to diagnose

And so, the only true way to diagnose this out of a clinical exam is to

this out of a clinical exam is to aspirate fluid from the joint. And then

aspirate fluid from the joint. And then what you see are these negatively, uh,

what you see are these negatively, uh, by refringent crystals. Um, you see

by refringent crystals. Um, you see white blood cells in there because of

white blood cells in there because of the inflammation, but it's the crystals

the inflammation, but it's the crystals that really highlight it. Uh, because

that really highlight it. Uh, because what you want to make sure is that it's

what you want to make sure is that it's not a septic joint. Um, but boy, if I I

not a septic joint. Um, but boy, if I I I can't tell you that I've ever

I can't tell you that I've ever aspirated an inflamed joint from gout

aspirated an inflamed joint from gout with, you know, without a patient

with, you know, without a patient punching you in the face. Um, so I mean

punching you in the face. Um, so I mean that is a very painful procedure, but

that is a very painful procedure, but technically that's how you diagnose

technically that's how you diagnose this. So acute inflammatory control, we

this. So acute inflammatory control, we got um appropriate doses of NSAIDs,

got um appropriate doses of NSAIDs, cultine, which is going to reduce the

cultine, which is going to reduce the diapodsis of the white blood cells to

diapodsis of the white blood cells to the area. It also prevents the

the area. It also prevents the replication of white blood cells as they

replication of white blood cells as they become activated. Um if somebody can't

become activated. Um if somebody can't take NSAIDs then that's where uh

take NSAIDs then that's where uh cortical steroids can be helpful at

cortical steroids can be helpful at reducing the inflammation in that area.

reducing the inflammation in that area. Um what you don't see in the acute

Um what you don't see in the acute management is alopurinol or faboxat

management is alopurinol or faboxat because because when you shift the

because because when you shift the concentrations

concentrations by inhibiting the formation of the uric

by inhibiting the formation of the uric acid um you can cause redistribution of

acid um you can cause redistribution of uric acid into different compartments

uric acid into different compartments and they can rec crystallize. So we

and they can rec crystallize. So we don't use that in the acute environment.

don't use that in the acute environment. We only use it in the preventative

We only use it in the preventative phase. So it's about six weeks after the

phase. So it's about six weeks after the acute flare then you can consider

acute flare then you can consider starting zanthinoxidase inhibitors and

starting zanthinoxidase inhibitors and patients not listen not taking six

patients not listen not taking six mercaptor purine or imiran

mercaptor purine or imiran um that is a life-threatening drug drug

um that is a life-threatening drug drug interaction that could cause significant

interaction that could cause significant bone marrow suppression there are rare

bone marrow suppression there are rare situations where that combination is

situations where that combination is used in patients with underlying

used in patients with underlying inflammatory bowel disease but that is

inflammatory bowel disease but that is not done by somebody who doesn't know

not done by somebody who doesn't know what they're doing. It's usually done by

what they're doing. It's usually done by a gastronologist with it more advanced

a gastronologist with it more advanced training.

>> Go ahead. >> Yeah, I was just going to add um with

>> Yeah, I was just going to add um with the bucksat, remember you've got a boxed

the bucksat, remember you've got a boxed warning for increased risk of heart

warning for increased risk of heart related death and just uh all cause

related death and just uh all cause death. So that's something to pay

death. So that's something to pay attention to and thinking about

attention to and thinking about coorbidities and choice of agent. Um

coorbidities and choice of agent. Um >> yep. Yeah. The uh rheumatologist like

>> yep. Yeah. The uh rheumatologist like fuxistat from a mechanistic standpoint

fuxistat from a mechanistic standpoint because it's clean. When you look at the

because it's clean. When you look at the mechanism of action of alipurol, it

mechanism of action of alipurol, it inhibits all kinds of other enzymes as

inhibits all kinds of other enzymes as well besides zanthine oxidase. And

well besides zanthine oxidase. And that's why alipurol has all these

that's why alipurol has all these problems including rashes and you have

problems including rashes and you have genetic polymorphism. So remember the

genetic polymorphism. So remember the genetic polymorphism 5801

genetic polymorphism 5801 uh would be the one that you would be

uh would be the one that you would be more predisposed to like SJS and TA and

more predisposed to like SJS and TA and that kind of stuff. So yeah, it's just

that kind of stuff. So yeah, it's just messy. But you know, everything's got a

messy. But you know, everything's got a double-edged sword. Osteoarthritis.

double-edged sword. Osteoarthritis. So this is where you have u too much

So this is where you have u too much inflammation which causes remodeling of

inflammation which causes remodeling of the cartilage and the bone joint

the cartilage and the bone joint surface. And so um it's different than

surface. And so um it's different than rheumatoid arthritis with it which is an

rheumatoid arthritis with it which is an autoimmune

autoimmune disease where the immune system is

disease where the immune system is attacking. Okay, very different. So

attacking. Okay, very different. So these tend to be weightbearing

these tend to be weightbearing joints.

joints. Um so you have joints in the spine, you

Um so you have joints in the spine, you have your uh knees, your hips being the

have your uh knees, your hips being the most common, especially with repetitive

most common, especially with repetitive use. And they can get swollen and have

use. And they can get swollen and have eusions. They be warm and they gets to

eusions. They be warm and they gets to be confusing as to the diagnosis. Is

be confusing as to the diagnosis. Is that an a septic joint or is that

that an a septic joint or is that osteoarthritis? But many times the

osteoarthritis? But many times the history of overuse, repetitive use, they

history of overuse, repetitive use, they tend to be overweight, those kinds of

tend to be overweight, those kinds of things tend to be in there. they're not

things tend to be in there. they're not having fevers, um that kind of stuff.

having fevers, um that kind of stuff. So, physical therapy, occupational

So, physical therapy, occupational therapy is key here because what that

therapy is key here because what that does is it strengthen the muscles um

does is it strengthen the muscles um around the joint to maintain the

around the joint to maintain the integrity of the joint and the joint

integrity of the joint and the joint movement. The next is you can do topical

movement. The next is you can do topical um analesics and including topical

um analesics and including topical NSAIDs or systemic analesia with NSAID

NSAIDs or systemic analesia with NSAID therapy. Um and this is where you might

therapy. Um and this is where you might even start picking up some of your COX 2

even start picking up some of your COX 2 selective agents. So not just celibre

selective agents. So not just celibre but also moxyam

but also moxyam um couttorlac those kind of agents that

um couttorlac those kind of agents that tend to be a little bit more coox 2

tend to be a little bit more coox 2 selective glucosamine chondroitin um if

selective glucosamine chondroitin um if you're going to use it has to be used

you're going to use it has to be used for three months it's really the

for three months it's really the chondroitin uh uh glucosamine component

chondroitin uh uh glucosamine component in it that really seems to offer the

in it that really seems to offer the benefit um but you know I've seen

benefit um but you know I've seen patients you know reduce the amount of

patients you know reduce the amount of naid use as a result. Is that a good

naid use as a result. Is that a good thing? Sure it is. but it's just not

thing? Sure it is. but it's just not going to happen right away. Very little

going to happen right away. Very little drug interactions, very little side

drug interactions, very little side effect profile with glucosamondroitin.

effect profile with glucosamondroitin. So, it's worth a shot. Um, heat cold

So, it's worth a shot. Um, heat cold therapy has to do with, you know, what

therapy has to do with, you know, what people what's going on. So, if it's an

people what's going on. So, if it's an acute swelling and inflammation, you

acute swelling and inflammation, you probably want some cold therapy that

probably want some cold therapy that reduces the blood flow, reduces the

reduces the blood flow, reduces the swelling and inflammation. Whereas if

swelling and inflammation. Whereas if you're stiff and you want to loosen the

you're stiff and you want to loosen the tissue, kind of get a little bit limber

tissue, kind of get a little bit limber with stretching and you know people are

with stretching and you know people are just stiff and having pain, then that's

just stiff and having pain, then that's where your heat therapy comes in.

where your heat therapy comes in. Um weight loss u for those joints and

Um weight loss u for those joints and then surgical repair, especially if none

then surgical repair, especially if none of the other things above are working.

of the other things above are working. All right, osteoporosis. So our bones

All right, osteoporosis. So our bones are constantly remodeling themselves.

are constantly remodeling themselves. That means the healthy bone is

That means the healthy bone is constantly breaking down and constantly

constantly breaking down and constantly being made. When the breaking down

being made. When the breaking down exceeds the rate of being made, slowly

exceeds the rate of being made, slowly over time you lose the density and then

over time you lose the density and then eventually that bone gets weak and with

eventually that bone gets weak and with enough force can break. Okay? And that's

enough force can break. Okay? And that's why you typically see it in the hips and

why you typically see it in the hips and those things like that because people

those things like that because people fall. Um, so this is where DEXA scans

fall. Um, so this is where DEXA scans come in and there's two types of scores

come in and there's two types of scores that you need to know. There's the dexa

that you need to know. There's the dexa scan t-core and zscore. Uh the t-core is

scan t-core and zscore. Uh the t-core is comparing the patient to a normal

comparing the patient to a normal otherwise healthy 30-year-old adults

otherwise healthy 30-year-old adults density. Okay, so that's this the

density. Okay, so that's this the standard deviation is uh less than you

standard deviation is uh less than you know has negative - 2.5. If you go zcore

know has negative - 2.5. If you go zcore that is comparing it to their peers. So

that is comparing it to their peers. So if you have a 56 year old, you know,

if you have a 56 year old, you know, female, then you're comparing it to

female, then you're comparing it to roughly another 56 year old female,

roughly another 56 year old female, similar height and weight, that kind of

similar height and weight, that kind of thing. Um, so zcores, t-cores serve two

thing. Um, so zcores, t-cores serve two different kind of perspectives.

different kind of perspectives. Um, because obviously a 75y old is not a

Um, because obviously a 75y old is not a 30-year-old, but that puts it in

30-year-old, but that puts it in perspective of how much they've lost too

perspective of how much they've lost too compared to what they probably were if

compared to what they probably were if you didn't know. Um this is where

you didn't know. Um this is where calcium vitamin D replacement becomes

calcium vitamin D replacement becomes important and you need appropriate

important and you need appropriate amounts and we usually have to dose that

amounts and we usually have to dose that in twice a day dosing because as I said

in twice a day dosing because as I said earlier you can only absorb so much at

earlier you can only absorb so much at one time and that's usually around 600

one time and that's usually around 600 milligrams of elemental calcium. Um and

milligrams of elemental calcium. Um and most people need about 600 milligrams of

most people need about 600 milligrams of vitamin D. Uh many of the bisphosinates

vitamin D. Uh many of the bisphosinates that are used for osteoporosis

that are used for osteoporosis prevention and or treatment have now

prevention and or treatment have now some combination of some calcium in it

some combination of some calcium in it to make it easier.

to make it easier. Um, exercise, weightbearing exercise can

Um, exercise, weightbearing exercise can help reduce that as long as it's not too

help reduce that as long as it's not too strenuous and they don't fall. Um,

strenuous and they don't fall. Um, reducing alcohol consumption and um,

reducing alcohol consumption and um, obviously calcium, vitamin D. Anything

obviously calcium, vitamin D. Anything else there?

else there? >> Um, you know, just remember if there's

>> Um, you know, just remember if there's some reason that they can't use a

some reason that they can't use a bisphosphinate, whether it's GI or maybe

bisphosphinate, whether it's GI or maybe renal, um, denosmab is your alternative,

renal, um, denosmab is your alternative, your rank L inhibitor. So, it's not a

your rank L inhibitor. So, it's not a bisphosphinate. It's different. uh

bisphosphinate. It's different. uh reloxifene also you know has its place

reloxifene also you know has its place or potential use in teride. So but domab

or potential use in teride. So but domab is probably your next most used um that

is probably your next most used um that you might see

you might see >> and even calcetonin nasal. So we talked

>> and even calcetonin nasal. So we talked about use of calcetonin um you know

about use of calcetonin um you know parental the IM subq injection for

parental the IM subq injection for hypercalcemia malignancy as a single

hypercalcemia malignancy as a single dose therapy but in in osteoporosis that

dose therapy but in in osteoporosis that would be your miaalin

would be your miaalin uh nasal spray. Um so yes just as Dr.

uh nasal spray. Um so yes just as Dr. Bolan mentioned terraparatide

Bolan mentioned terraparatide that's your um parathyroid hormone

that's your um parathyroid hormone analoges and then your denucimab which

analoges and then your denucimab which is going to be a monoconal antibbody

is going to be a monoconal antibbody that regulates the activity or lifespan

that regulates the activity or lifespan of the uh osteoclast

of the uh osteoclast um is another um option to um you know

um is another um option to um you know consider especially if you can't

consider especially if you can't tolerate the bisphosates which you know

tolerate the bisphosates which you know definitely have problems.

definitely have problems. All right good stuff. All right, moving

All right good stuff. All right, moving on to let me just see if there's any

on to let me just see if there's any questions since we're doing okay here.

Uh, no comments on the monocone antibbody for um Alzheimer's. The

antibbody for um Alzheimer's. The dukeab, I forgot. I I don't even know

dukeab, I forgot. I I don't even know how you say it. No, ain't going to be

how you say it. No, ain't going to be there. Too controversial. Not going to

there. Too controversial. Not going to be on the exam. Remember, it's got to be

be on the exam. Remember, it's got to be wellestablished standards of practice.

wellestablished standards of practice. No debate. Not going to be on the test.

No debate. Not going to be on the test. Tamsyloin cannot be given via PEG tube.

Tamsyloin cannot be given via PEG tube. What drug can we switch to? Um

I don't know the answer to that and I guess it depends on what you're trying

guess it depends on what you're trying to treat. Is this I guess for BPH? If

to treat. Is this I guess for BPH? If it's for BPH,

it's for BPH, um you know, yes, you can switch to

um you know, yes, you can switch to Docas and Trazisonin. Um but just

Docas and Trazisonin. Um but just obviously keep in mind the risks. So you

obviously keep in mind the risks. So you have to just weigh the risk of benefit.

have to just weigh the risk of benefit. Uh but I can't I don't know off the top

Uh but I can't I don't know off the top of my head. I apologize if you can push

of my head. I apologize if you can push those down a peg tube. Uh Amanda's

those down a peg tube. Uh Amanda's asking where does uh Aventity fit into

asking where does uh Aventity fit into osteoporosis treatment?

osteoporosis treatment? Um I don't know the answer to that off

Um I don't know the answer to that off the top of my head. Apologize. Do you

the top of my head. Apologize. Do you know?

know? >> Sorry. I was trying to figure out the

>> Sorry. I was trying to figure out the answer to the other one. Um

>> well, we'll just look it up. I don't have it. I don't have an answer off the

have it. I don't have an answer off the top of my head. What was the other one

top of my head. What was the other one again? The

again? The >> uh

>> uh I think I heard I' I've recently heard

I think I heard I' I've recently heard about this, but I don't I haven't looked

about this, but I don't I haven't looked into it in depth. So,

into it in depth. So, >> yeah.

>> yeah. >> Sorry. I don't have a good answer for

>> Sorry. I don't have a good answer for that. Again, guys, listen. So, when new

that. Again, guys, listen. So, when new drugs come out or new transitions to

drugs come out or new transitions to medications or any kind of other adjunct

medications or any kind of other adjunct is not going to be on a test, it has to

is not going to be on a test, it has to it's going to take at least 12 months or

it's going to take at least 12 months or longer to make it to an an exam. And it

longer to make it to an an exam. And it has to have a very specific

has to have a very specific uh uh agreed upon location for its use.

uh uh agreed upon location for its use. And if that does not exist, and I'll

And if that does not exist, and I'll have to double check it. I I did

have to double check it. I I did remember that drug uh coming out, but I

remember that drug uh coming out, but I I I'm it's not going to be on the test.

I I'm it's not going to be on the test. So try to separate. Remember, you're

So try to separate. Remember, you're playing a game, okay? And the mindset of

playing a game, okay? And the mindset of the board exams is not the mindset of

the board exams is not the mindset of cutting edge, you know, new information

cutting edge, you know, new information and new guidelines that just come out.

and new guidelines that just come out. So, it it just takes that long. I don't

So, it it just takes that long. I don't know how else to stress that. Um, but um

know how else to stress that. Um, but um it seems to come up a lot. You guys ask

it seems to come up a lot. You guys ask that qu a lot of these questions about

that qu a lot of these questions about new information a lot. So, just resist

new information a lot. So, just resist the temptation of going down rabbit

the temptation of going down rabbit trails in these holes um because they're

trails in these holes um because they're not it's not going to it's you're

not it's not going to it's you're wasting time from a board exam

wasting time from a board exam perspective. Okay. Bell's palsy. So in

perspective. Okay. Bell's palsy. So in this case, the problem is cranial nerve

this case, the problem is cranial nerve 7, which is the nerve that comes right

7, which is the nerve that comes right basically out of the side of your head

basically out of the side of your head here through a little hole and it

here through a little hole and it basically goes like this on one side.

basically goes like this on one side. You've got another one on this side. So

You've got another one on this side. So that's why you get unilateral facial

that's why you get unilateral facial paralysis for the most part. Um that

paralysis for the most part. Um that also involves the forehead. So the whole

also involves the forehead. So the whole lateral part of the face is compromised

lateral part of the face is compromised which is very important because if the

which is very important because if the forehead as I mentioned in the clinical

forehead as I mentioned in the clinical presentation is being spared like I can

presentation is being spared like I can still do this but this part of my face

still do this but this part of my face is not working then this is a stroke

is not working then this is a stroke okay if this is not working it tends to

okay if this is not working it tends to be Bell's palsy huge difference

be Bell's palsy huge difference obviously one's tpa Hey, what is

obviously one's tpa Hey, what is steroids?

steroids? Very big difference. So, um, so the

Very big difference. So, um, so the diagnosis and the physical exam is key

diagnosis and the physical exam is key in their presentation so that you make

in their presentation so that you make sure you're treating the right problem.

sure you're treating the right problem. So, if it does involve the eye, which

So, if it does involve the eye, which means your muscle, you can't close your

means your muscle, you can't close your eye, then they need usually need a eye

eye, then they need usually need a eye patch so that you don't scratch the

patch so that you don't scratch the eyeball and cause a corial abrasion or

eyeball and cause a corial abrasion or ulcer, but they also can dry out their

ulcer, but they also can dry out their eye. I mean, if you try to hold your

eye. I mean, if you try to hold your eyes open, you will like not be able to

eyes open, you will like not be able to do it. Your eyes will force you to

do it. Your eyes will force you to blink, and that's because your eyes will

blink, and that's because your eyes will start to dry out, and that's only after

start to dry out, and that's only after a few seconds. So, these patients need a

a few seconds. So, these patients need a lot a lot of repeated eye drops. And you

lot a lot of repeated eye drops. And you hope to God that the steroids, if you

hope to God that the steroids, if you can start them within 72 hours, plus or

can start them within 72 hours, plus or minus, that's very controversial about

minus, that's very controversial about the use of antivirals. Um, but really

the use of antivirals. Um, but really the steroids so that you try to reduce

the steroids so that you try to reduce inflammation on that nerve to try to

inflammation on that nerve to try to free that nerve's activity back up

free that nerve's activity back up before it dies. There are some patients

before it dies. There are some patients who have permanent

who have permanent Bell's palsy and it never regain

Bell's palsy and it never regain function. So steroids, steroids,

function. So steroids, steroids, steroids very early on as early within

steroids very early on as early within 72 hours if you can get it started that

72 hours if you can get it started that quickly. Uh, cluster headaches, so

quickly. Uh, cluster headaches, so migraines and headaches. Cluster

migraines and headaches. Cluster headaches are kind of a little weird and

headaches are kind of a little weird and that it's usually causes conjunctable

that it's usually causes conjunctable injection. They usually have runny eyes,

injection. They usually have runny eyes, runny nose with a headache. That's the

runny nose with a headache. That's the classic pattern. This is where lidocaine

classic pattern. This is where lidocaine intraasal spray can be helpful.

intraasal spray can be helpful. Certainly the tripan still are

Certainly the tripan still are beneficial and steroids. Okay. In the

beneficial and steroids. Okay. In the acute for prevention um it's your

acute for prevention um it's your calcium channel blockers particularly

calcium channel blockers particularly non-hydropodine

non-hydropodine um calcium channel blockers. Migraine

um calcium channel blockers. Migraine headaches the traditional classic. This

headaches the traditional classic. This is where you have sort of the basogenic

is where you have sort of the basogenic edema. It's affecting the uh the

edema. It's affecting the uh the trigeminal nerves of the brain which

trigeminal nerves of the brain which have huge nerve that has three different

have huge nerve that has three different branches um that goes throughout our

branches um that goes throughout our entire skull. Um many times those are

entire skull. Um many times those are the things that are impacted uh by it.

the things that are impacted uh by it. It's associated with the prodrome. They

It's associated with the prodrome. They will have any kind of they can smell

will have any kind of they can smell things, see things, paristhesas.

things, see things, paristhesas. Everybody has a little bit different

Everybody has a little bit different one. Um it can last for hours if not

one. Um it can last for hours if not days. There's really no workup that

days. There's really no workup that needs to be done. If it's a first-time

needs to be done. If it's a first-time diagnosis and it's unusual presentation,

diagnosis and it's unusual presentation, sometimes people will get a CT scan of

sometimes people will get a CT scan of the brain just to make sure something

the brain just to make sure something else isn't going on. Um, but on an exam,

else isn't going on. Um, but on an exam, they're going to be very clear history,

they're going to be very clear history, you know, and want you to treat it. So,

you know, and want you to treat it. So, there's acute management and then

there's acute management and then there's the prophylaxis. In the acute

there's the prophylaxis. In the acute phase, there is more than one way to

phase, there is more than one way to skin this cat. Okay? So there are a lot

skin this cat. Okay? So there are a lot of different regimens out there that you

of different regimens out there that you can use for abortive treatments. Um you

can use for abortive treatments. Um you know tripans are classically in that DHA

know tripans are classically in that DHA um products slightly are still used not

um products slightly are still used not as much but are probably more this true

as much but are probably more this true migraine patient that has done well with

migraine patient that has done well with it and doesn't have any underlying

it and doesn't have any underlying cardiovascular disease. Um but what most

cardiovascular disease. Um but what most of the time breaks the people's cycle is

of the time breaks the people's cycle is some combination of treatment

some combination of treatment um where you give like prochlorazine

um where you give like prochlorazine or metacopramide with a little bit of

or metacopramide with a little bit of benadryil which partially just gets

benadryil which partially just gets their mind off of the headache and then

their mind off of the headache and then they kind of get a little tired and they

they kind of get a little tired and they start relaxing. If you can get them to

start relaxing. If you can get them to sleep sometimes that will just calm down

sleep sometimes that will just calm down the edema and the stress associated with

the edema and the stress associated with it. And then of course give NSAIDs to

it. And then of course give NSAIDs to reduce the vasogenic edema um that's

reduce the vasogenic edema um that's happening and the inflammation to the

happening and the inflammation to the nerves around those blood vessels in the

nerves around those blood vessels in the brain and around the cranial uh uh

brain and around the cranial uh uh trigeminal nerve. Once you get to the

trigeminal nerve. Once you get to the preventative phase, now you're thinking

preventative phase, now you're thinking about anticonvulsants

about anticonvulsants um in particular like drugs like

um in particular like drugs like topyramate calcium channel blockers in

topyramate calcium channel blockers in particular the non-diar calcium channel

particular the non-diar calcium channel blockers non selective bay blockers in

blockers non selective bay blockers in particular propanol

particular propanol because you're getting the uh beta 2

because you're getting the uh beta 2 antagonism that causes constriction. And

antagonism that causes constriction. And the reason it's propanol and not natal

the reason it's propanol and not natal is propanol is lipopilic and actually

is propanol is lipopilic and actually get into the blood brain barrier through

get into the blood brain barrier through it into the central nervous system.

it into the central nervous system. Whereas natal can't do that. We don't

Whereas natal can't do that. We don't use a tennoltopol for headaches. It is

use a tennoltopol for headaches. It is propanol. Um when you get beyond that

propanol. Um when you get beyond that you're still having problems. Botox

you're still having problems. Botox injections

injections um have been used. Um there's new class

um have been used. Um there's new class of drugs the uh CGRP

of drugs the uh CGRP antagonist. Um, and then there's also

antagonist. Um, and then there's also even over-the-counter u magnesium

even over-the-counter u magnesium hydroxide or not hydroxide oxide

hydroxide or not hydroxide oxide supplements. You just got to be careful

supplements. You just got to be careful how much magnesium you take. Um, but I

how much magnesium you take. Um, but I done some I did some of my training in a

done some I did some of my training in a migraine clinic and we would use a lot

migraine clinic and we would use a lot of magnesium supplements and it seems to

of magnesium supplements and it seems to be very effective uh for that. And part

be very effective uh for that. And part of the part of that uh has to do with

of the part of that uh has to do with the interference or blocking of the um

the interference or blocking of the um calcium mediate effects which affect

calcium mediate effects which affect neurotransmitter release that sort of

neurotransmitter release that sort of triggers some of this process.

triggers some of this process. Uh Dr. Bolan, anything there?

Uh Dr. Bolan, anything there? >> No, I don't think so.

>> No, I don't think so. >> All right. So, we're doing pretty good.

>> All right. So, we're doing pretty good. Got about another 25 or so, 30 minutes

Got about another 25 or so, 30 minutes before we need we'll take questions.

before we need we'll take questions. Uh high altitude sickness. So this is

Uh high altitude sickness. So this is when you go um too rapidly up in

when you go um too rapidly up in elevation uh into the atmosphere uh

elevation uh into the atmosphere uh which then changes where the uh oxygen

which then changes where the uh oxygen concentration has changed in the tension

concentration has changed in the tension and it changes what happens to the blood

and it changes what happens to the blood vessels in your brain and it also

vessels in your brain and it also affects your breathing um where you

affects your breathing um where you regulate your CO2. Uh and these patients

regulate your CO2. Uh and these patients go through different phases. So you

go through different phases. So you start developing high altitude sickness

start developing high altitude sickness where you get a little bit of a

where you get a little bit of a headache, you feel like off, you know,

headache, you feel like off, you know, you have a little bit of a taxis. Some

you have a little bit of a taxis. Some people start getting confused and then

people start getting confused and then they can start getting nauseous. Once

they can start getting nauseous. Once you start developing edema, okay, where

you start developing edema, okay, where your brain is swelling, okay, from all

your brain is swelling, okay, from all the dilation of the blood vessels and

the dilation of the blood vessels and those things, then um these patients

those things, then um these patients start getting they start vomiting, they

start getting they start vomiting, they get really confused and that is called

get really confused and that is called haste um or high alitude cerebral edema.

haste um or high alitude cerebral edema. If it starts to cause shortness of

If it starts to cause shortness of breath and stuff like that, now you're

breath and stuff like that, now you're into HAPE, high altitude pulmonary

into HAPE, high altitude pulmonary edema. And that is an acute life both

edema. And that is an acute life both cerebral edema and pulmonary edema are

cerebral edema and pulmonary edema are acute life-threatening conditions that

acute life-threatening conditions that require emergent rapid descent down the

require emergent rapid descent down the mountain quickly. Um so if it starts to

mountain quickly. Um so if it starts to happen you need to recognize it and

happen you need to recognize it and there is a self test that you can do uh

there is a self test that you can do uh and you should be aware of if especially

and you should be aware of if especially if you've never been in a high altitude

if you've never been in a high altitude environment for the first time. um you

environment for the first time. um you should consider recognizing the symptoms

should consider recognizing the symptoms of this because if you don't and you

of this because if you don't and you continue to climb, you're going to get

continue to climb, you're going to get yourself in trouble. And that's why some

yourself in trouble. And that's why some people when they climb mountains,

people when they climb mountains, they'll acclimate to an area for a day

they'll acclimate to an area for a day or two and then progress on to the next

or two and then progress on to the next level and then stop and then progress on

level and then stop and then progress on to the next level so that their body

to the next level so that their body makes the adjustments. It's the sudden

makes the adjustments. It's the sudden transfer. So terminating ascent and

transfer. So terminating ascent and beginning the descent adding on

beginning the descent adding on supplemental oxygen if you have it. Uh

supplemental oxygen if you have it. Uh if they are really symptomatic and

if they are really symptomatic and having significant CNS changes like

having significant CNS changes like cerebral edema then they need hyperaric

cerebral edema then they need hyperaric therapy. Um if you have any evidence of

therapy. Um if you have any evidence of cerebral edema then it is a rapid

cerebral edema then it is a rapid descent by at least 2 to 4,000 feet. Um

descent by at least 2 to 4,000 feet. Um you can use steroids and this drug of

you can use steroids and this drug of choice is dexamethasone.

choice is dexamethasone. Um there are um bags that you can put

Um there are um bags that you can put people on that create sort of like a

people on that create sort of like a hyperaric

hyperaric sa uh situation but also helps you to

sa uh situation but also helps you to remove the patient from the environment

remove the patient from the environment quickly. Um now for prevention uh pre-

quickly. Um now for prevention uh pre- uh elevation you can take acettoolamide

uh elevation you can take acettoolamide which basically puts you in a state of

which basically puts you in a state of acidosis

acidosis and so you start to uh breathe faster

and so you start to uh breathe faster and get rid of the CO2 which changes the

and get rid of the CO2 which changes the uh concentrations of the CO2 get you

uh concentrations of the CO2 get you acclimated. Some people can take

acclimated. Some people can take pre-mptively take a little bit of

pre-mptively take a little bit of dexamethasone to kind of prevent some of

dexamethasone to kind of prevent some of the edema uh from happening. Uh so those

the edema uh from happening. Uh so those are two options for the preventative

are two options for the preventative side.

side. All right, moving on to intraraanial

All right, moving on to intraraanial pressure management. So you have ICP

pressure management. So you have ICP that's elevated and it can be from a lot

that's elevated and it can be from a lot of reasons. It can be from menitis, it

of reasons. It can be from menitis, it can be from trauma, it can be from an es

can be from trauma, it can be from an es schemic insult with the swelling.

schemic insult with the swelling. Anything that raises the intraanial

Anything that raises the intraanial pressure can affect uh numerous

pressure can affect uh numerous mechanism uh physiologic parameters in

mechanism uh physiologic parameters in your body. in particularly you start

your body. in particularly you start developing um altered mental status so

developing um altered mental status so confusion. Second you start having a

confusion. Second you start having a widened pulse pressure that means that

widened pulse pressure that means that your systolic blood pressure is much

your systolic blood pressure is much bigger than your diastolic blood

bigger than your diastolic blood pressure. So you have a very large

pressure. So you have a very large systolic to diastolic ratio and then you

systolic to diastolic ratio and then you see brada cardia. So widening pulse

see brada cardia. So widening pulse pressure with breda cardia um and then

pressure with breda cardia um and then altered respirations. Where I see it

altered respirations. Where I see it most commonly is in traumatic brain

most commonly is in traumatic brain injury where there is a subdural

injury where there is a subdural hematoma or epidural hematoma or

hematoma or epidural hematoma or subacoid traumatic subactoid hemorrhage

subacoid traumatic subactoid hemorrhage where the blood is accumulating and it's

where the blood is accumulating and it's starting to press on the tissue and then

starting to press on the tissue and then they eventually herniate their brain

they eventually herniate their brain stem if you don't stop it. Uh so how do

stem if you don't stop it. Uh so how do you fix that? Well, we try to do

you fix that? Well, we try to do everything possible to reduce ICP. That

everything possible to reduce ICP. That includes uh you know reclining the

includes uh you know reclining the patient by 30 degrees, not laying them

patient by 30 degrees, not laying them flat or putting them in reverse

flat or putting them in reverse trendelenburgg where their feet are down

trendelenburgg where their feet are down and their head is up to just allow you

and their head is up to just allow you know gravity to help you with drainage.

know gravity to help you with drainage. Keeping their neck align not like this.

Keeping their neck align not like this. Okay. Um and so that you facilitate the

Okay. Um and so that you facilitate the blood vessels being in an anatomical

blood vessels being in an anatomical position to maximize uh flow. Um if that

position to maximize uh flow. Um if that doesn't work, you got hypertonic saline

doesn't work, you got hypertonic saline and you got ma manitol that you can

and you got ma manitol that you can consider using until you can get

consider using until you can get surgical intervention. Uh if there is no

surgical intervention. Uh if there is no neurosurgery,

neurosurgery, uh I will drill a hole in your head. Um

uh I will drill a hole in your head. Um so

so I'm not kidding. I mean, we basically

I'm not kidding. I mean, we basically drill a hole right here, pull out a

drill a hole right here, pull out a portion of your skull and let the

portion of your skull and let the decompress the nerve because otherwise

decompress the nerve because otherwise if your brain herniates, you're going to

if your brain herniates, you're going to die um instantaneously and there's no

die um instantaneously and there's no fixing it. Um if you have a neurosurgeon

fixing it. Um if you have a neurosurgeon around or you can get the patient to a

around or you can get the patient to a neurosurgeon, then obviously a

neurosurgeon, then obviously a cranottomy and the uh extraction of the

cranottomy and the uh extraction of the blood is going to be the greatest way or

blood is going to be the greatest way or something to put an ICP monitor in to

something to put an ICP monitor in to drain off the fluid for whatever the

drain off the fluid for whatever the reason it is. So, these are more acute

reason it is. So, these are more acute life-threatening situations that require

life-threatening situations that require acute interventions. Traumatic brain

acute interventions. Traumatic brain injury without signs and symptoms of ICP

injury without signs and symptoms of ICP where you're having those manifestations

where you're having those manifestations like the Cushings trial that I

like the Cushings trial that I mentioned. Um, these patients um where

mentioned. Um, these patients um where there's actual damage to the brain and

there's actual damage to the brain and they have concussive symptoms and

they have concussive symptoms and usually blood um in that area. uh then

usually blood um in that area. uh then these patients usually get uh anti-

these patients usually get uh anti- convulsant prophylaxis for 7 days. It's

convulsant prophylaxis for 7 days. It's not any longer. It's a unique duration.

not any longer. It's a unique duration. Most commonly phenotin, phosphenito or

Most commonly phenotin, phosphenito or uh levitatoram or keera. Uh most people

uh levitatoram or keera. Uh most people have been migrating to levitraetam but

have been migrating to levitraetam but they're all correct answers. So

they're all correct answers. So phenotin, phosphenettoine, levitacetam

phenotin, phosphenettoine, levitacetam 7 days uh TBI prophylaxis

7 days uh TBI prophylaxis pseudotumor cerebri this is a fake tumor

pseudotumor cerebri this is a fake tumor because they manifest with these extreme

because they manifest with these extreme headaches, changes in vision usually um

headaches, changes in vision usually um they can have um uh uh dipopia, loss of

they can have um uh uh dipopia, loss of vision. They can start having loss of

vision. They can start having loss of pial vision uh visual uh fields loss.

pial vision uh visual uh fields loss. And the reason for this is that they're

And the reason for this is that they're making basically the accumulation of CSF

making basically the accumulation of CSF fluid. So they they're having decreased

fluid. So they they're having decreased reabsorption and too much production. So

reabsorption and too much production. So there's this flow of CSF through the

there's this flow of CSF through the brain where the output is exceeding the

brain where the output is exceeding the amount being removed. And so it starts

amount being removed. And so it starts to back up, back up, back up, and back

to back up, back up, back up, and back up. Well, remember the fluid is

up. Well, remember the fluid is surrounding your brain and the there's

surrounding your brain and the there's these um sistns or you know sulkai in

these um sistns or you know sulkai in your brain that it's filling around

your brain that it's filling around keeping it sort of absorbed. But but

keeping it sort of absorbed. But but your nerves, your optic nerves to your

your nerves, your optic nerves to your eyeballs are attached to your brain. So

eyeballs are attached to your brain. So that fluid starts pushing out and people

that fluid starts pushing out and people can start having papadeema

can start having papadeema um which is you can only see that by

um which is you can only see that by looking in their in the back of their

looking in their in the back of their eye with the uh opthalmoscope uh and

eye with the uh opthalmoscope uh and then they start having vision changes

then they start having vision changes because of that. So if they have vision

because of that. So if they have vision changes and they have these headaches um

changes and they have these headaches um you have to keep in mind uh that this is

you have to keep in mind uh that this is potentially going to happen. They can go

potentially going to happen. They can go blind if you don't treat it.

blind if you don't treat it. So how do you treat acutely?

So how do you treat acutely? Acettozolomide

Acettozolomide um is one of the treatments of choice um

um is one of the treatments of choice um because again that makes them sort of

because again that makes them sort of decreases the production of CSF fluid

decreases the production of CSF fluid but also starts to potentially make them

but also starts to potentially make them hyperventilate a little bit which

hyperventilate a little bit which constricts the vessels. On top of that

constricts the vessels. On top of that we do a therapeutic lumbar puncture and

we do a therapeutic lumbar puncture and we drain off the CSF fluid. Literally, I

we drain off the CSF fluid. Literally, I sit there and drain off all the CSF

sit there and drain off all the CSF fluid until their CSF pressures get back

fluid until their CSF pressures get back to normal range. Um, and so I just keep

to normal range. Um, and so I just keep dumping it, dumping it, and dumping it

dumping it, dumping it, and dumping it until it comes down.

until it comes down. >> Um, and there where I trained at Johns

>> Um, and there where I trained at Johns Hopkins, we had so many cerebrum

Hopkins, we had so many cerebrum cerebri patients that there was a cere

cerebri patients that there was a cere pseudotumor cerebri clinic. These

pseudotumor cerebri clinic. These patients just came and get lumbar

patients just came and get lumbar punctures. That's how bad it is. Um so

punctures. That's how bad it is. Um so prevention um there's acettoolamide oral

prevention um there's acettoolamide oral therapies that you can use chloralone uh

therapies that you can use chloralone uh cortical steroids in particular those

cortical steroids in particular those that don't have uh mineral cortical

that don't have uh mineral cortical activity like dexamethasone and methyl

activity like dexamethasone and methyl predinisolone predominantly. Um if

predinisolone predominantly. Um if they're still having problems with their

they're still having problems with their vision then optic nerve sheath

vision then optic nerve sheath defenistration can sometimes happen to

defenistration can sometimes happen to relieve some of that pressure on the

relieve some of that pressure on the optic nerve.

optic nerve. Um

Um but yeah, you don't want to miss this

but yeah, you don't want to miss this one. They can go blind. Multiple

one. They can go blind. Multiple sclerosis. This is where our an

sclerosis. This is where our an autoimmune mediated event where

autoimmune mediated event where basically you're attacking the

basically you're attacking the mileination

mileination of the neurons or the axons. And so

of the neurons or the axons. And so these typically occur in younger

these typically occur in younger otherwise healthy women. Um they usually

otherwise healthy women. Um they usually present with fatigue, these weird

present with fatigue, these weird paristhesas like nerve sensations. They

paristhesas like nerve sensations. They can have muscle spasicity. uh they can

can have muscle spasicity. uh they can start seeing double um again those are

start seeing double um again those are similar symptoms of some patients with

similar symptoms of some patients with pseudoti but there's no headache as is

pseudoti but there's no headache as is as much associated with it there are

as much associated with it there are different categories there's the

different categories there's the relapsing remitting MS and then there's

relapsing remitting MS and then there's like here there's the progressive

like here there's the progressive relapsing primary progressive and

relapsing primary progressive and secondary progressive um which just

secondary progressive um which just really have to do with how they're

really have to do with how they're cycling and their lesions um so an MRI

cycling and their lesions um so an MRI is usually necessary to see these

is usually necessary to see these lesions um in the brain and monitor

lesions um in the brain and monitor their um activity over time because

their um activity over time because that's our goal is to reduce the lesion

that's our goal is to reduce the lesion activity and the progression. So when

activity and the progression. So when they get these acute MS flares

they get these acute MS flares basically the immune system is revved

basically the immune system is revved up. So we're going to give something to

up. So we're going to give something to suppress the immune system. The most

suppress the immune system. The most common first line treatment is high dose

common first line treatment is high dose steroids most commonly methyl

steroids most commonly methyl prediniscolone

prediniscolone for three days followed by oral

for three days followed by oral therapies for two weeks and then you

therapies for two weeks and then you titrate down for another week and create

titrate down for another week and create sort of a taper. Um there are a number

sort of a taper. Um there are a number of demarss out there now that are being

of demarss out there now that are being used um interferon especially for some

used um interferon especially for some of the other versions there. Um I think

of the other versions there. Um I think this is a little bit slightly lower

this is a little bit slightly lower yield for the exam but we wanted to make

yield for the exam but we wanted to make sure we kind of hit it. If they are

sure we kind of hit it. If they are having the muscle spasticity blephin

having the muscle spasticity blephin taanadine probably the two more common

taanadine probably the two more common ones backfin probably being the most

ones backfin probably being the most common drug of choice used in this

common drug of choice used in this situation and if those don't work or

situation and if those don't work or there's some reason you can't use it

there's some reason you can't use it then bzzodazzipines like dazipan.

then bzzodazzipines like dazipan. Dr. And uh anything that you have to add

Dr. And uh anything that you have to add for any of the stuff that I've been

for any of the stuff that I've been talking

talking >> I know it's more the acute stuff

>> I know it's more the acute stuff sometimes that but

sometimes that but um okay peripheral neuropathy so it is

um okay peripheral neuropathy so it is what it is the peripheral you know

what it is the peripheral you know extremities usually having some

extremities usually having some manifestation of neuropathic changes so

manifestation of neuropathic changes so they usually have these burning tingling

they usually have these burning tingling sensations or it could just be come

sensations or it could just be come right just depends on the degree and

right just depends on the degree and what caused the damage. So there's like

what caused the damage. So there's like you know in Dr. Bolan's world, you know,

you know in Dr. Bolan's world, you know, with a lot of diabetics, diabetic

with a lot of diabetics, diabetic neuropathy. Um, there's drug induced

neuropathy. Um, there's drug induced peripheral neuropathies. We saw a lot of

peripheral neuropathies. We saw a lot of those back in the day of the HIV drugs

those back in the day of the HIV drugs and RTI, you know, u, the D drugs, um,

and RTI, you know, u, the D drugs, um, like stabine and those medications we

like stabine and those medications we don't use as much anymore. Um, there's

don't use as much anymore. Um, there's also even the vinka alkaloids and your

also even the vinka alkaloids and your taxes, which are your chemotherapy

taxes, which are your chemotherapy agents. So those are dose limiting

agents. So those are dose limiting toxicities the neuropathy. So these are

toxicities the neuropathy. So these are real scenarios that can happen to people

real scenarios that can happen to people and they describe them in different

and they describe them in different ways. Uh most commonly anticonvulsants

ways. Uh most commonly anticonvulsants gabapentin and pregablin are used also

gabapentin and pregablin are used also lowd dose tcas. So low dose being

lowd dose tcas. So low dose being somewhere in that 10 to 50 milligram

somewhere in that 10 to 50 milligram window. Once you get to 100 milligrams

window. Once you get to 100 milligrams of like amatipptalene and norptalene

of like amatipptalene and norptalene these things now you're getting into

these things now you're getting into anti-depressant doses where you start

anti-depressant doses where you start running the risk of QRS widening where

running the risk of QRS widening where you need to monitor levels and or at

you need to monitor levels and or at least get a EKG. You don't need to do

least get a EKG. You don't need to do levels and you don't need to do EKGs on

levels and you don't need to do EKGs on patients with lowdose neuropathy uh with

patients with lowdose neuropathy uh with treatment by TCA

treatment by TCA trigeminal neuralgia. So the trigeminal

trigeminal neuralgia. So the trigeminal nerve is what I was mentioning earlier

nerve is what I was mentioning earlier in certain migraines. Um it's a massive

in certain migraines. Um it's a massive nerve cranial nerve that comes out is

nerve cranial nerve that comes out is just huge. It's got three different

just huge. It's got three different branches to it. Um so it goes to

branches to it. Um so it goes to different parts of obviously the skull.

different parts of obviously the skull. Um and but when patients get trigeminal

Um and but when patients get trigeminal neuralgia it is ex excruciating severe

neuralgia it is ex excruciating severe like lightning bolt pain. I mean these

like lightning bolt pain. I mean these patients come in almost screaming in

patients come in almost screaming in pain. Um and so anticvulsants are the

pain. Um and so anticvulsants are the drug. So think about it, it's a nerve.

drug. So think about it, it's a nerve. So if I want to suppress nerve function,

So if I want to suppress nerve function, I'm going to do something to slow down

I'm going to do something to slow down nerve conduction, right? So the drug of

nerve conduction, right? So the drug of choice on a board exam would be

choice on a board exam would be carbomasopene.

carbomasopene. Other is oxarbazopene. If you can't for

Other is oxarbazopene. If you can't for some reason use carbomasopene like if

some reason use carbomasopene like if you have phiccogenetic issues 50 uh 5701

you have phiccogenetic issues 50 uh 5701 right

right that's a back yeah

>> um if that doesn't work back because they will get some muscle spasm from it

they will get some muscle spasm from it and then um uh uh Botox injections into

and then um uh uh Botox injections into the nerves or you just go into surgical

the nerves or you just go into surgical gamma knife basically going straight

gamma knife basically going straight into and strategically cutting certain

into and strategically cutting certain nerves. Uh microvascular decompressions

nerves. Uh microvascular decompressions and other procedures have been used but

and other procedures have been used but carbomasopene is probably you're going

carbomasopene is probably you're going to probably stop at these first two

to probably stop at these first two bullets here. Um it's more recognizing

bullets here. Um it's more recognizing the face and the cranial that trigeminal

the face and the cranial that trigeminal nerve. Moving on to restless leg. So

nerve. Moving on to restless leg. So this is where there's a movement

this is where there's a movement disorder and most commonly from some

disorder and most commonly from some dopamineergic issue or dysfunction or

dopamineergic issue or dysfunction or they have iron pretty significant iron

they have iron pretty significant iron deficiency. So yeah, iron deficiency

deficiency. So yeah, iron deficiency that didn't make sense to me but it's

that didn't make sense to me but it's actually one of the treatments is

actually one of the treatments is replacing them and evaluating from iron

replacing them and evaluating from iron deficiency anemia and then treating and

deficiency anemia and then treating and replacing it first because that's the

replacing it first because that's the easiest thing because it treats two

easiest thing because it treats two different things.

different things. Um, if that doesn't work, you got

Um, if that doesn't work, you got dopamine agonist that you take at night.

dopamine agonist that you take at night. And again, as I mentioned, it's a much

And again, as I mentioned, it's a much smaller dose than what you would use for

smaller dose than what you would use for Parkinson's disease.

Parkinson's disease. Um, so just keep that in mind. Um,

Um, so just keep that in mind. Um, pretty straightforward. Absant seizures.

Some of you are probably going, you got the uh uh what's his name? Uh a

you got the uh uh what's his name? Uh a Napoleon Dynamite look.

Napoleon Dynamite look. That's an Absson seizure. If you look

That's an Absson seizure. If you look like Napoleon Dynamite, you are having

like Napoleon Dynamite, you are having an absent seizure. So you absent

an absent seizure. So you absent seizures are you are absent

seizures are you are absent absent for these little periods. They're

absent for these little periods. They're sudden onset. They're not convulsing,

sudden onset. They're not convulsing, but they happen for a few seconds and

but they happen for a few seconds and then they just pick right back up with

then they just pick right back up with what they were doing like it didn't

what they were doing like it didn't happen.

happen. So obviously if you're doing something

So obviously if you're doing something like walking downstairs or driving a

like walking downstairs or driving a car,

car, hopefully you're not doing surgery.

hopefully you're not doing surgery. Yeah. You know, some something that

Yeah. You know, some something that requires your cognitive move, you know,

requires your cognitive move, you know, system to be intact. Uh this would be a

system to be intact. Uh this would be a problem. And uh the drug of choice for

problem. And uh the drug of choice for most of exams is obviously ethosomide.

most of exams is obviously ethosomide. This probably even extends back to the

This probably even extends back to the old naplax days, but but don't forget

old naplax days, but but don't forget about lamotrogene and valproic acid as

about lamotrogene and valproic acid as um especially those that have a little

um especially those that have a little bit of other unusual findings associated

bit of other unusual findings associated with it, but they'll have repeated

with it, but they'll have repeated periods of being absent without

periods of being absent without convulsions. Um it's sort of a classic

convulsions. Um it's sort of a classic um

um case

case drug induced seizures. So

drug induced seizures. So you have to think about toxicology

you have to think about toxicology predominantly in this situation.

predominantly in this situation. Obviously, not all drugs can cause

Obviously, not all drugs can cause seizures in a toxin area. It can just

seizures in a toxin area. It can just lower the seizure threshold. So, I mean

lower the seizure threshold. So, I mean there's drugs like wellutrin or

there's drugs like wellutrin or bupropion, tramodol, clausipene, some of

bupropion, tramodol, clausipene, some of the stimulants that at normal doses,

the stimulants that at normal doses, especially in a patient with already

especially in a patient with already risk factors, it can lower the seizure

risk factors, it can lower the seizure threshold enough just to flip it. But

threshold enough just to flip it. But certainly if you overdose, especially

certainly if you overdose, especially with Wellbutrin or Tramodol,

with Wellbutrin or Tramodol, that's high risk. Very high risk. If you

that's high risk. Very high risk. If you have any thing in the case where there

have any thing in the case where there is drug uh overdose or consumption and

is drug uh overdose or consumption and you don't know anything about what's

you don't know anything about what's going on and nobody else knows because

going on and nobody else knows because they patients just arrived, EMS got

they patients just arrived, EMS got called out and and they're seizing, you

called out and and they're seizing, you never ever ever

never ever ever give an anti-comvulsant.

give an anti-comvulsant. Never ever.

Never ever. Not fastenitoine, not phenotin, not

Not fastenitoine, not phenotin, not keera since keer may everybody seems to

keera since keer may everybody seems to want to put it in the water now. No,

want to put it in the water now. No, it's a benzoazipene. Hands down. Period.

it's a benzoazipene. Hands down. Period. End of discussion. The exception to the

End of discussion. The exception to the rule is if you have like a TB patient

rule is if you have like a TB patient who was suicidal and they found bottles

who was suicidal and they found bottles of his TB drugs laying around and one of

of his TB drugs laying around and one of them is isid, then that is the only time

them is isid, then that is the only time you would ever treat a seizure with a

you would ever treat a seizure with a vitamin.

highdose vitamin B6 paradoxine is the only thing that's going to help that

only thing that's going to help that patient outside of that benzo benzo

patient outside of that benzo benzo benzo benzo if you have an IV give uh

benzo benzo if you have an IV give uh laorazzipam if you have no IV because

laorazzipam if you have no IV because they're con convulsing and you can't get

they're con convulsing and you can't get an IV started then you know hit them in

an IV started then you know hit them in the muscle and the best drug with a more

the muscle and the best drug with a more consistent phiccoinetic profile and more

consistent phiccoinetic profile and more rapid absorption is madazzylam in that

rapid absorption is madazzylam in that situation over adavan

situation over adavan So, they should not put both drugs on

So, they should not put both drugs on the answer choices. That would be

the answer choices. That would be largely inappropriate. But if you have

largely inappropriate. But if you have both on there and they have an IV,

both on there and they have an IV, you're going for Adavan because it's not

you're going for Adavan because it's not just the onset, but it's also the

just the onset, but it's also the duration so they don't come back out of

duration so they don't come back out of it.

it. Um,

I think that as I was making this slide or I was having a seizure because

or I was having a seizure because that should say status epileptic.

Oh, dear God. Pretty sure I was having a seizure. I'm

Pretty sure I was having a seizure. I'm just going to say I was having a

just going to say I was having a seizure. That's my excuse for that one.

seizure. That's my excuse for that one. I mean, I don't even know what that is.

I mean, I don't even know what that is. I was looking like, what is that? What

I was looking like, what is that? What is that? That's a person having a

is that? That's a person having a seizure.

seizure. >> All right, guys. So, status epilepticus,

>> All right, guys. So, status epilepticus, what it is that show up? So, you see you

what it is that show up? So, you see you see on there it says a continuous

see on there it says a continuous ongoing

ongoing single seizure for five minutes or more

single seizure for five minutes or more is status. Okay.

is status. Okay. Also,

Also, if you have a traditional tonic clonic

if you have a traditional tonic clonic seizure that lasts, you know, 2 minutes,

seizure that lasts, you know, 2 minutes, which is kind of normal, and they just

which is kind of normal, and they just stop like they normally do,

stop like they normally do, and then they go into a post-dictal

and then they go into a post-dictal phase where they're confused, altered,

phase where they're confused, altered, blah, blah, blah, but then within

blah, blah, blah, but then within another two to three minutes or

another two to three minutes or whatever, they have another seizure or

whatever, they have another seizure or in between that they never came back to

in between that they never came back to and had another seizure.

and had another seizure. That is status epilepticus until proven

That is status epilepticus until proven otherwise.

otherwise. Now, you got to be really careful

Now, you got to be really careful because some people can still be seizing

because some people can still be seizing and not convulsing.

and not convulsing. So if somebody goes through the typical

So if somebody goes through the typical tonicclonic seizure and then stops and

tonicclonic seizure and then stops and then they're like grunting and making

then they're like grunting and making all this noise afterwards in the

all this noise afterwards in the post-dictal phase, I will watch them and

post-dictal phase, I will watch them and if they're not slowly coming back to a

if they're not slowly coming back to a little bit enough to where they're

little bit enough to where they're starting to breathe a little bit more,

starting to breathe a little bit more, then I'm going to intubate the patient

then I'm going to intubate the patient to protect the airway. But I'm also

to protect the airway. But I'm also looking at their eyes and seeing if

looking at their eyes and seeing if their eyes are still looking like

their eyes are still looking like they're seizing. So that's happened

they're seizing. So that's happened numerous times. So when in doubt air on

numerous times. So when in doubt air on the side of precaution because status

the side of precaution because status epilepticus has a carries a high

epilepticus has a carries a high mortality uh associated with it. Um

mortality uh associated with it. Um and so you know again um drug of choice

and so you know again um drug of choice and status epilepticus IV uh Adavan

and status epilepticus IV uh Adavan um IM medazzelam if you have the ability

um IM medazzelam if you have the ability to load somebody and it's not drug

to load somebody and it's not drug toxicity uh phosphenito is probably the

toxicity uh phosphenito is probably the preferred it's the prod drug to phenotin

preferred it's the prod drug to phenotin and the dosing member is based off

and the dosing member is based off phenotin equivalent so it's 20

phenotin equivalent so it's 20 milligrams of phenotin equivalents per

milligrams of phenotin equivalents per kilogram

kilogram loading dose but you can give it faster.

loading dose but you can give it faster. So remember phenotin can only be given

So remember phenotin can only be given at 50 milligrams per minute whereas

at 50 milligrams per minute whereas phosphenatorine can be given at three

phosphenatorine can be given at three times that so 150 milligrams per minute.

times that so 150 milligrams per minute. Um and so you can give it much faster if

Um and so you can give it much faster if you don't have an IV you can also give

you don't have an IV you can also give it I am okay. Um rectal dasopam is

it I am okay. Um rectal dasopam is traditionally used if you have nothing

traditionally used if you have nothing else and nothing else is working or many

else and nothing else is working or many times this is what the patient and the

times this is what the patient and the patient's family have at home um and

patient's family have at home um and they give the patient all right moving

they give the patient all right moving on to acute eskeemic stroke. So you have

on to acute eskeemic stroke. So you have some sort of cerebral vascular occlusion

some sort of cerebral vascular occlusion which is causing death to a area of the

which is causing death to a area of the tissue and depending on where the you

tissue and depending on where the you know vessel is going will influence what

know vessel is going will influence what neurologic manifestation is being seen

neurologic manifestation is being seen but it's usually a focal progressive

but it's usually a focal progressive neurode deficit that is acute onset and

neurode deficit that is acute onset and is typically unilateral not bilateral I

is typically unilateral not bilateral I can't move my arms it is you know facial

can't move my arms it is you know facial asymmetries facial drooping slur speech

asymmetries facial drooping slur speech can't move my left arm, can't move my

can't move my left arm, can't move my right arm only, or I can't move my leg,

right arm only, or I can't move my leg, something like that. Okay. Um, if

something like that. Okay. Um, if they're within a 4 and 1/2 hour window,

they're within a 4 and 1/2 hour window, and these rules have been relaxed a

and these rules have been relaxed a little bit, but you know, the

little bit, but you know, the manufacturer says within three hours,

manufacturer says within three hours, guidelines say four and a half hours of

guidelines say four and a half hours of the onset of last being normal. So, the

the onset of last being normal. So, the story has got to be very good. Okay? So

story has got to be very good. Okay? So if they went to bed normal and they woke

if they went to bed normal and they woke up eight or nine hours later,

up eight or nine hours later, you have to assume that the last time of

you have to assume that the last time of normal was the night before. Okay? And

normal was the night before. Okay? And so they usually fall outside the window

so they usually fall outside the window of treatment for alttoplace therapy at

of treatment for alttoplace therapy at that point. Um and so they get a bolus

that point. Um and so they get a bolus and then they get an infusion over an

and then they get an infusion over an hour. This dosing is different than in

hour. This dosing is different than in STEMI. It's also different than in sub

STEMI. It's also different than in sub massive PE. So just keep in mind the

massive PE. So just keep in mind the dosing is a little bit different. But

dosing is a little bit different. But always rule out hypoglycemia because

always rule out hypoglycemia because hypoglycemia can be a stroke mimic.

hypoglycemia can be a stroke mimic. Sometimes that's a trick question. Um,

Sometimes that's a trick question. Um, so treat their glucose, keep it in

so treat their glucose, keep it in normal range, treat the blood pressure.

normal range, treat the blood pressure. Remember, if the blood pressure is

Remember, if the blood pressure is greater than 185, systolic or diastolic

greater than 185, systolic or diastolic over 110, that's a contraindication

over 110, that's a contraindication until you get the blood pressure down

until you get the blood pressure down and adequately controlled. Glucose

and adequately controlled. Glucose levels should be around 140 to 180

levels should be around 140 to 180 window. A TIA is different from a trans

window. A TIA is different from a trans a acute eskeemic stroke and that TIA

a acute eskeemic stroke and that TIA will have some resolution of symptoms

will have some resolution of symptoms usually over the first couple hours but

usually over the first couple hours but all the way up into the first day. If

all the way up into the first day. If you have some resolution and improvement

you have some resolution and improvement so they have this focal neurologic

so they have this focal neurologic deficit

deficit um and but yet they're starting to have

um and but yet they're starting to have improvement in symptoms then alt place

improvement in symptoms then alt place because of the risk of eskeemic

because of the risk of eskeemic hemorrhage I'm sorry converting to

hemorrhage I'm sorry converting to hemorrhage is high you don't want to

hemorrhage is high you don't want to probably use that in situation then you

probably use that in situation then you can start them on aspirin therapy at

can start them on aspirin therapy at that time or if they're allergic to

that time or if they're allergic to aspirin then copitigril and then admit

aspirin then copitigril and then admit them for a stroke workup for secondary

them for a stroke workup for secondary prevention of like you know do they have

prevention of like you know do they have corateed artery

corateed artery uh stenosis and aththeroscerosis or you

uh stenosis and aththeroscerosis or you know what why did they have a TIA came

know what why did they have a TIA came from somewhere

from somewhere now if they hemorrhagically convert

now if they hemorrhagically convert which eskeemic strokes can because the

which eskeemic strokes can because the tissue is dying and the blood vessel

tissue is dying and the blood vessel ruptures or they're on anti-coagulants

ruptures or they're on anti-coagulants or something else and they had a

or something else and they had a spontaneous

spontaneous stroke

stroke now you've got to be worried about

now you've got to be worried about increased intraanial pressure issues

increased intraanial pressure issues where they may have the Cushings triad

where they may have the Cushings triad where they have you know the wide pulse

where they have you know the wide pulse pressure, bradic cardia, altered

pressure, bradic cardia, altered respirations and then start losing

respirations and then start losing protection of their airway um and they

protection of their airway um and they need decompression of that pressure. So

need decompression of that pressure. So typically this is why we when somebody

typically this is why we when somebody comes in with stroke like symptoms we

comes in with stroke like symptoms we always always do a head CT

always always do a head CT uh because you don't want to give the

uh because you don't want to give the hemorrhagic stroke tpa. I mean you're

hemorrhagic stroke tpa. I mean you're going to make it significantly worse. Um

going to make it significantly worse. Um so in these situations you also want to

so in these situations you also want to regulate blood pressure within reason

regulate blood pressure within reason and this is where we have to be careful.

and this is where we have to be careful. If we block drop the blood pressure too

If we block drop the blood pressure too much you may hypo proferuse the brain.

much you may hypo proferuse the brain. Uh if this is a hemorrhagic stroke from

Uh if this is a hemorrhagic stroke from a ruptured aneurysm or a subacoid

a ruptured aneurysm or a subacoid hemorrhage then this is where uh

hemorrhage then this is where uh neotapene

neotapene is indicated in the first 96 hours of

is indicated in the first 96 hours of the onset to prevent neurologic

the onset to prevent neurologic complications basically from the spasms

complications basically from the spasms of the vessel. Um, neotoopene is not

of the vessel. Um, neotoopene is not used it's a uh the hydroparidian calcium

used it's a uh the hydroparidian calcium channel blocker that is not used for um

channel blocker that is not used for um it is not used for uh hypertension. Uh

it is not used for uh hypertension. Uh it's only used for subaractoid

it's only used for subaractoid hemorrhage. If you are actively still

hemorrhage. If you are actively still bleeding and you're on a you know warin

bleeding and you're on a you know warin or a doak or something then that's where

or a doak or something then that's where drugs like Kentra

drugs like Kentra um come into play until you can get

um come into play until you can get surgical evacuation.

surgical evacuation. Vertigo um so the problem with vertigo

Vertigo um so the problem with vertigo is obviously people feel off they the

is obviously people feel off they the room is spinning. They may have

room is spinning. They may have vestibular problems. Um the biggest

vestibular problems. Um the biggest issue is whether it's peripheral or

issue is whether it's peripheral or central. So if it's central, we are

central. So if it's central, we are concerned about a potential stroke

concerned about a potential stroke because a stroke to the posterior aspect

because a stroke to the posterior aspect of your brain and specifically the uh

of your brain and specifically the uh cerebellum can increase your risk of

cerebellum can increase your risk of presenting as vertigo. And so that's a

presenting as vertigo. And so that's a stroke like manifestation. Whereas

stroke like manifestation. Whereas peripheral vertigo like uh BPPV or

peripheral vertigo like uh BPPV or something like that has to do with

something like that has to do with usually position of their head. And so

usually position of their head. And so people that are like on a you know boat

people that are like on a you know boat or something and the boat is rocking so

or something and the boat is rocking so they're looking forward

they're looking forward their eyes are looking one way receiving

their eyes are looking one way receiving input this way their ears and the

input this way their ears and the semic-ircular canals are moving in a

semic-ircular canals are moving in a different direction. There's a m

different direction. There's a m mismatch and it causes them to get uh

mismatch and it causes them to get uh these symptoms and they can obviously

these symptoms and they can obviously vomit. So obviously central vertigo is a

vomit. So obviously central vertigo is a whole different can of worms. that's a

whole different can of worms. that's a neurologic evaluation. It may even

neurologic evaluation. It may even require TPA. Um, you're probably not

require TPA. Um, you're probably not going to get that question. You're going

going to get that question. You're going to be getting the peripheral vertigo

to be getting the peripheral vertigo question where you use kind of the anti-

question where you use kind of the anti- histaminic drugs, scopalamine. Um, you

histaminic drugs, scopalamine. Um, you have your antihistamines. Um, and even

have your antihistamines. Um, and even um, you know, dasopam if it's if it's

um, you know, dasopam if it's if it's bad enough. Okay. Well, we finished a

bad enough. Okay. Well, we finished a couple minutes late, but we did good. We

couple minutes late, but we did good. We got through a lot of stuff. So we

got through a lot of stuff. So we remember we did GI,

remember we did GI, renal, geriatric and neuro. So let's

renal, geriatric and neuro. So let's look at see what some of the questions

look at see what some of the questions that we have here. Uh migraine propanol

that we have here. Uh migraine propanol and risean is there a max dose of risean

and risean is there a max dose of risean in my memory if my memory serves? I

in my memory if my memory serves? I don't know off the top of my head. Um

don't know off the top of my head. Um I I don't know. I just I don't know the

I I don't know. I just I don't know the answer to that question. Um,

answer to that question. Um, where propanol use comes in to be a

where propanol use comes in to be a problem

problem is if you're going to use

is if you're going to use So, so here's where

So, so here's where uh here's where it is an issue with

uh here's where it is an issue with tripans and

tripans and uh the DHA, you know, agents, the old

uh the DHA, you know, agents, the old school, uh because they're going to

school, uh because they're going to cause constriction, right? So, what are

cause constriction, right? So, what are you doing with propanol? So beta, it's a

you doing with propanol? So beta, it's a non- selective beta blocker. So you're

non- selective beta blocker. So you're antagonizing beta 1 receptor that's not

antagonizing beta 1 receptor that's not helping me with the headache. But the

helping me with the headache. But the antagonism of the beta 2 receptor is

antagonism of the beta 2 receptor is causing constriction because remember

causing constriction because remember beta 2 activation causes dilation of the

beta 2 activation causes dilation of the blood vessels. Um so so Jordan is saying

blood vessels. Um so so Jordan is saying that rizotan is 30 milligrams a day I do

that rizotan is 30 milligrams a day I do believe and 10 milligrams

believe and 10 milligrams per dose. So, but if you think about

per dose. So, but if you think about mechanistically what's happening and why

mechanistically what's happening and why they're care wanting to be careful is

they're care wanting to be careful is because you don't want to over constrict

because you don't want to over constrict that almost get kind of like unopposed

that almost get kind of like unopposed constriction like you would see with

constriction like you would see with cocaine and beta blocker use

uh let's see

let's see >> Dr. Bat um to go back to the question

>> Dr. Bat um to go back to the question earlier. Yes,

earlier. Yes, >> that's Romaab,

>> that's Romaab, which I just I didn't recognize the

which I just I didn't recognize the brand name of that. Um, but that one is

brand name of that. Um, but that one is fairly new. It's bone building. It is

fairly new. It's bone building. It is definitely for your severe patients.

definitely for your severe patients. >> Um, so you're thinking fracture with uh

>> Um, so you're thinking fracture with uh lower than negative -2.5.

lower than negative -2.5. Um,

Um, >> yeah. Not going to be on the test.

>> yeah. Not going to be on the test. >> Yeah. Um,

>> Yeah. Um, >> not on this test.

>> not on this test. >> And not with a cardiovascular history.

>> And not with a cardiovascular history. if you did happen to see it. So not

if you did happen to see it. So not definitely not in that patient that has

definitely not in that patient that has any significant cardiovascular history.

any significant cardiovascular history. >> Okay. Uh so looks like we have uh

>> Okay. Uh so looks like we have uh schemic stroke. Can you go over the

schemic stroke. Can you go over the absolute contraindications?

absolute contraindications? >> Okay. Um, so there's so I clinically you

>> Okay. Um, so there's so I clinically you should look it up and never fully rely

should look it up and never fully rely on your memory. Um, because in the midst

on your memory. Um, because in the midst of a real situation, you don't want to

of a real situation, you don't want to all humans can make errors. So I just

all humans can make errors. So I just want to say that because I that is my

want to say that because I that is my standard of practice. I always always go

standard of practice. I always always go through the checklist

through the checklist um because it's just too dangerous to

um because it's just too dangerous to miss it. However, you know, obviously

miss it. However, you know, obviously the blood pressure is the first and

the blood pressure is the first and foremost thing that most people tend to

foremost thing that most people tend to focus on and that's your blood pressure

focus on and that's your blood pressure that you know systolic is greater than

that you know systolic is greater than 185 over 110. And really where it's a

185 over 110. And really where it's a contraindication to using tpa at all is

contraindication to using tpa at all is if you can't get the blood pressure

if you can't get the blood pressure under control and keep it under control.

under control and keep it under control. What you do not want as it relates to

What you do not want as it relates to blood pressure issues is the cyclical

blood pressure issues is the cyclical up and down effect of blood pressure.

up and down effect of blood pressure. You do not want that because when it

You do not want that because when it comes down and you're like, "Oh, the

comes down and you're like, "Oh, the number looks great. Go ahead and give it

number looks great. Go ahead and give it and then it like pops back up in the

and then it like pops back up in the middle of the infusion." Um, it is that

middle of the infusion." Um, it is that peak transition that causes the

peak transition that causes the hemorrhagic conversion or risk of

hemorrhagic conversion or risk of hemorrhagic conversion. Remember, you

hemorrhagic conversion. Remember, you have you have tissue that's dying. the

have you have tissue that's dying. the cells and the cell walls uh and those of

cells and the cell walls uh and those of the vasculature are weak. Um you also

the vasculature are weak. Um you also need to rule out he uh hypoglycemia or

need to rule out he uh hypoglycemia or hyperglycemia.

hyperglycemia. Um you have INRs that are greater than

Um you have INRs that are greater than 1.7 if they're on patients with the low

1.7 if they're on patients with the low platelet counts or thrombocytoenia.

platelet counts or thrombocytoenia. Um you have a recent uh surgical

Um you have a recent uh surgical procedures or trauma where there was you

procedures or trauma where there was you know significant bleeding a uh previous

know significant bleeding a uh previous uh stroke especially in the last three

uh stroke especially in the last three months and again because of the

months and again because of the hemorrhagic conversion risk of the dead

hemorrhagic conversion risk of the dead tissue still remodeling itself.

tissue still remodeling itself. Um having seizures tip those a seizure

Um having seizures tip those a seizure is actually sometimes considered a

is actually sometimes considered a really a relative contraation.

really a relative contraation. Um and then um if you have an NIH I'll

Um and then um if you have an NIH I'll say some other comments. If you have

say some other comments. If you have patients over 80 patients who have an

patients over 80 patients who have an NIH stroke scale of 26 or more and you

NIH stroke scale of 26 or more and you have a massive stroke like and your NIH

have a massive stroke like and your NIH stroke scale is that high, I probably

stroke scale is that high, I probably would not give it. Um because the risk

would not give it. Um because the risk of hemorrhagic conversion is going to be

of hemorrhagic conversion is going to be high and the outcomes are probably not

high and the outcomes are probably not going to be good. uh or if I did, it

going to be good. uh or if I did, it would only be in the context of the

would only be in the context of the patient's family. The patient wouldn't

patient's family. The patient wouldn't be able to consent at at an NIH stroke

be able to consent at at an NIH stroke scale of 26. Um the patient's family

scale of 26. Um the patient's family would have to um give consent. But I

would have to um give consent. But I think that, you know, so those are some

think that, you know, so those are some of the major uh ones. But the board exam

of the major uh ones. But the board exam is not going to

is not going to um put a whole list of items in there

um put a whole list of items in there and make you pick, you know, some

and make you pick, you know, some minutia um like that. Let's see. Are

minutia um like that. Let's see. Are thyide diuretics worse than uh

thyide diuretics worse than uh precipitating gout than loops? It seems

precipitating gout than loops? It seems like

like a second. It seems like thyids are

a second. It seems like thyids are mentioned more, but it can happen with

mentioned more, but it can happen with both. So it can happen with both. So

both. So it can happen with both. So remember both uh loop diuretics and

remember both uh loop diuretics and thyide diuretics

thyide diuretics um have to get secreted into the tubule

um have to get secreted into the tubule and they have they they work on the

and they have they they work on the luminal side. So they have to get inside

luminal side. So they have to get inside the tubule through secretion at usually

the tubule through secretion at usually the level of the proximal renal tubule.

the level of the proximal renal tubule. that location of the proximal renal

that location of the proximal renal tubule are where the uric acid trans

tubule are where the uric acid trans transporters are present. So they

transporters are present. So they basically utilize

basically utilize similar pathways.

similar pathways. Um I because more people are on thy

Um I because more people are on thy diuretics

diuretics in general especially because of

in general especially because of underlying hypertension

underlying hypertension um they get more attention uh as causing

um they get more attention uh as causing it uh because of the o use and the

it uh because of the o use and the volume of people compared to the volume

volume of people compared to the volume of people on loops. So I'm not saying

of people on loops. So I'm not saying loops are obviously very common too but

loops are obviously very common too but if you look at the number of people on

if you look at the number of people on thighides compared to loops it's much

thighides compared to loops it's much greater.

greater. Okay

Okay what other questions do we have?

Anybody having a seizure or maybe you already loaded yourself with phenotin or

already loaded yourself with phenotin or phosphenotin or adaban or mazzlam or all

phosphenotin or adaban or mazzlam or all four of them.

four of them. Maybe Kerra,

Everybody's hung up and gone to sleep, drooling on themselves.

drooling on themselves. Uh, Dr. Boland mentioned SSRIs and

Uh, Dr. Boland mentioned SSRIs and hyponetriia.

Yes. So, do you want to do you want any

So, do you want to do you want any comments on it? I can answer it, too.

comments on it? I can answer it, too. >> I mean, just it's it's one of those

>> I mean, just it's it's one of those things. Um

things. Um I

I >> it's as I yeah I mean it

>> it's as I yeah I mean it >> I've seen it only couple of times where

>> I've seen it only couple of times where it was like truly suspected. A lot of

it was like truly suspected. A lot of times it's another ideology, but it is

times it's another ideology, but it is um one of those drug interactions when

um one of those drug interactions when you think about an elderly patient. A

you think about an elderly patient. A lot of times they'll be on an SSRI,

lot of times they'll be on an SSRI, whether it's for

whether it's for >> some dep like depression or anxiety. Um

>> some dep like depression or anxiety. Um and you can see that and usually it's

and you can see that and usually it's not

not the the cases I've seen anyway is not as

the the cases I've seen anyway is not as significant.

significant. >> Yeah, it's

>> Yeah, it's >> of a drop. It's very mild usually

>> of a drop. It's very mild usually >> and it's almost always in the pattern of

>> and it's almost always in the pattern of SIADH or syndrome of inappropriate

SIADH or syndrome of inappropriate antidiuretic hormone like pattern. So

antidiuretic hormone like pattern. So what you would essentially do is either

what you would essentially do is either switch the antid-depressant

switch the antid-depressant and see if it goes away or put them on

and see if it goes away or put them on free water um

free water um free water uh restriction um or minimize

free water uh restriction um or minimize some of that. You know, some people need

some of that. You know, some people need free water restriction. I see these

free water restriction. I see these people walking around with, you know,

people walking around with, you know, milk jugs of free water. And I go, you

milk jugs of free water. And I go, you ain't healthy. I'm just telling you

ain't healthy. I'm just telling you right now. In fact, you're probably

right now. In fact, you're probably killing yourself because drinking all

killing yourself because drinking all that water is does nothing except

that water is does nothing except redilute your electrolytes and could

redilute your electrolytes and could make you start having seizures.

make you start having seizures. So, drink up.

So, drink up. You don't need that much water.

You don't need that much water. All right. Very good review, doctors.

All right. Very good review, doctors. Thank you so much. Getting ready for a

Thank you so much. Getting ready for a shift in the morning. God bless. All

shift in the morning. God bless. All right. Take care, Ruth. Have a good

right. Take care, Ruth. Have a good shift.

shift. Uh, let's see. Amanda, I just wanted to

Uh, let's see. Amanda, I just wanted to make sure I heard that correct. You did

make sure I heard that correct. You did hear it correct. You are not

hear it correct. You are not hallucinating.

hallucinating. You are not delusional.

You are not delusional. You did hear that SSRI have been

You did hear that SSRI have been associated with SIADH and hyponetriia.

associated with SIADH and hyponetriia. Um, back in the day they used to say

Um, back in the day they used to say that it maybe with some of the longer

that it maybe with some of the longer acting SSRIs.

acting SSRIs. Um, I know that like um,

Um, I know that like um, Paxel and by the way Paxel is another

Paxel and by the way Paxel is another one too with within special populations

one too with within special populations that uh, you don't want to use like in

that uh, you don't want to use like in pregnant patients because it's the one

pregnant patients because it's the one that's associated with PPHA PPHN

persistent pulmonary hypertension of the newborn.

newborn. Start started having a seizure there

Start started having a seizure there myself.

Paxel is evil. Yeah, it's it's got some bad rap. I will agree. It does not have

bad rap. I will agree. It does not have good rap. Poor

good rap. Poor >> P.

>> P. >> All right. What else, guys? You guys are

>> All right. What else, guys? You guys are rock stars. Everybody excited about

rock stars. Everybody excited about taking your test. Like just gung-ho.

If you drink enough, uh, if you drink enough, it the test is

uh, if you drink enough, it the test is always much better. I mean, you can

always much better. I mean, you can laugh your way through the exam.

laugh your way through the exam. I'm just kidding. Don't do that.

I'm just kidding. Don't do that. >> No,

>> No, that won't go well.

that won't go well. >> All right, guys. Y'all are quiet, so I

>> All right, guys. Y'all are quiet, so I think that's it. So, we're going to end

think that's it. So, we're going to end early. And, uh, thank you guys for your

early. And, uh, thank you guys for your participation. I'm serious. Uh,

participation. I'm serious. Uh, hopefully you find these useful. We have

hopefully you find these useful. We have another session where we will

another session where we will I think dive into

I think dive into um geez uh we have psych and I think

um geez uh we have psych and I think bioatistics

bioatistics >> I think

>> I think >> little rapid review on bioatistics man

>> little rapid review on bioatistics man that's everybody's favorite that's the

that's everybody's favorite that's the way to go out

way to go out >> psych pulmonary and EBM

>> psych pulmonary and EBM >> yeah pulmonary

>> yeah pulmonary psych

psych and some EBM man we are going out in

and some EBM man we are going out in style all right guys have a good one

style all right guys have a good one Take care. Bye.

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YouTube Transcript:Session 5 - Live Rapid Review for BPS Exams