DIP Episode 599 - The Clutch Dementia Podcast (Step 1-3)

All right, welcome. My name is divine. This is episode 599 of the divine intervention podcasts into these podcasts. We're gonna be going over a topic I like to call dementia, right? This is gonna be the clutch dementia podcast. This podcast is super high yield. You're gonna see the stuff tested on your exams. Step one, step two, step three, level one, level two, level three. So you might as well just pay attention and get the points down. All right, let's jump right into it. So what if they give you a question about an individual, you know, that comes to visit the physician for example, physical. And you're told that this individual is asking about, you know, things he can do, you know, they usually tell you that give you a big thing about a big family history of dementia or cognitive impairment. And then they'll ask you which of the following interventions would most likely reduce the patient's risk of developing a dementia or cognitive impairment. Basically on your exams when you see questions like that, the smart play is to think of answers that involve controlling metabolic risk factors, right? So, you know, things like diabetes, high blood pressure, you know, hyperliplidemia, exercising, exercising is a big one. The love on the US MLE is certainly reduces the person's risk of cognitive decline, you know, eating a healthy diet. Again, those are the only things that really reduce your risk of developing cognitive impairment.

All right, especially exercise exercises is a big one to know for the US ML Es. But, you know, I'm sure many of you have probably heard of the term type three diabetes with Alzheimer's, right? Having an insulin resistance has a strong in the brain has a very strong association with people developing dementia. Now, one thing I just mentioned here, some people are like, ooh, the one talked about cognitive impairment, cognitive impairment. What's the deal with cognitive impairment on your exam? Well, here's the thing. Because many people they mess up cognitive impairment versus straight up dementia on the exams. Again, many of these resources like to emphasize this criteria, that criteria, this criteria, that criteria. No, don't worry about those things. Let me just tell you the simple trick on your exams. For patients having issues with memory, but they have, they are okay with their D to their activities. The activities of daily living, they can still cook for themselves. You know, they're having some memory problems, but they can still cook for themselves, they can still clean, they can still interact with other people. They are not struggling with activities of daily living. That person probably has a mild cognitive impairment, probably has a mild cognitive impairment. And then, what if they give you a question about a person that is struggling with the activities of daily living, the person, you know, scores like a 20 out of 30 on a minimal status exam.

And the person is, you know, being forgetful on their way back from work and all those things. And they ask you which of the following is the most appropriate next step in pharmacotherapy? Well, I would really hope that you should be thinking of giving an acetylcholinesteries inhibitor. And this person I just described probably has Alzheimer's dementia. The first line pharmacotherapy for Alzheimer's is an acetylcholinesteries inhibitor like donepesil or galantamine or rivestigmen. Donepesil, galantamine or rivestigmen. And let me let you in on a secret, actually. Let me let you in on a secret. Do you know that giving acetylcholinesteries inhibitors is pretty much the way you treat every kind of dementia on the USMEL exams? There's like two exceptions to that rule and I will discuss them. But for the most part, most dementia syndromes on the USME Ls, Louis Body Dementia Alzheimer's dementia, Vascular dementia, you should give them acetylcholinesteries inhibitors. They may not respond as well as the person with Alzheimer's, but the treatment of most dementia syndromes on the USME Ls is to give an acetylcholinesteries inhibitor. And one thing I want to say here is this, the exceptions to this rule I'm giving you are going to be things like frontal temporal dementia. Honestly, there's no great treatment for frontal temporal dementia. Cerocolnesteries inhibitors don't do squat for those people. And then also the other one, the Waqewer and Wabley folks, right?

The people with no more pressure had your cephalus. I would hope you're not giving those people acetylcholinesteries inhibitors when you can just put a VP shunt of intraculopyritoneal shunt and resolve their problems. Right? So that's kind of high you to know. So one thing that I know some of you may be wondering in your mind is, why do we use acetylcholinesteries inhibitors to treat Alzheimer's? Well, the thing is, in Alzheimer's, one thing that is destroyed is a brain structure known as the bison nucleus of mean art. The bison nucleus of mean art, you know, at least it's dysfunctional. So because you have dysfunction of that part of the brain, you're going to have low levels of acetylcholine in the brain. So it will be helpful to kind of perk that up by giving an acetylcholinesteries inhibitor. Right? In fact, now that I mentioned that our friends at the NBM Es, they love you to know these anatonic associations with some of these dimensions, you know, like Alzheimer's, you know, there's so many of you know, decreased activity of the bison nucleus of minor to show it's in every on key deck known to mankind. But another thing, there are a bunch of other things they actually love to test, right? So remember in Alzheimer's, you're going to have atrophy of the hippocampus, they can have like destruction of the hippocampus. That's why they have memory problems. Because remember, the hippocampus is basically your memory center in the brain. Right?

And then another thing you may see in Alzheimer's is this thing known as hydrocephalus X-Vaco. Right? So because the cortex, the cerebral cortex shrinks in size, the ventricles look bigger in comparison. Right? I just kind of think of it this way. If you that is us, you know, if you're feeling yourself that, oh, I'm a five foot nine, I'm five foot nine, I'm five foot nine. If you're five foot nine, and you stand around most common individuals, it's not a big deal. You look very tall in comparison. But if you're standing around a bunch of like MB5s, you know, MB centers, you're going to look pretty small. Right? So it's like in comparison to something else, just because something of a different size has is placed around you. So the thing is if you have a lot of corticol atrophy, then the ventricles will look bigger in comparison. We call that phenomenon hydrocephalus X-Vaco. Hydrocephalus X-Vaco on the exams. What are some other neuro anatomical associations you want to know with your dementia? So what do you want to know that people that have no more pressure hydrocephalus, they're going to have ventricleomegaly. They're going to have ventricleomegaly. The ventricles are going to be big. But remember, those people when you do a lumber puncture, their symptoms are going to improve dramatically. But in addition, it's helpful to know that when you do a lumber puncture, this will have a normal CSF opening pressures.

Please don't make the mistake of saying that they will have a high CSF opening pressures. That'll be a terrible idea. High CSF opening pressures, we find it in people that have idiopathic intra-cranial hypertension, which we call pseudo-tomorcerybri. So the macerarybri has the same pathophases as MPH, decrease CSF absorption at the arachnoid ground relations. But when you do a lumber puncture, people that have MPH, they're going to have normal CSF opening pressures, people that have IH, idiopathic intra-cranial hypertension, they're going to have increased CSF opening pressures. Big diff, very important to know for your exams. And then I guess some other anatomical things to know with Alzheimer's as well. They like to test some of these genetic stuff. Remember that the Epo E form mutation is a serial that increase risk of pressing developing Alzheimer's. But if you have Epo E2, it's protective against Alzheimer's dementia. And then don't forget your presenylene things. So presenylene one, which we find on chromosome 14, presenylene two which we find on chromosome one, these things are going to raise your risk of early onset Alzheimer's. Although to be honest with you, most people that have Alzheimer's, it's just a sporadic thing that happens. There's no like genetic thing going on.

Although don't forget that people also that have a down syndrome, because they have three copies of chromosome 21, they have three copies of the amyloid precursor protein, so they certainly have an increased risk of Alzheimer's. In fact, around each 40, most people that have down syndrome already have Alzheimer's dementia. And again, remember, when accumulating the brain in Alzheimer's, your extracellular amyloid plaques, those neurofibreillary tangles. And the USML is, they love to mess people up on exams. They will use the term extracellular versus use the term intracellular versus intracellular. So remember the cells we find in the brain are the neurons. These amyloid plaques are not intracellular accumulations. They are extracellular accumulations. But the neurofibreillary tangles, what are they? Are they intracellular or extracellular? Well, I hope you're seeing that they are intracellular. They are intracellular. They are within the neurons. They are intraneuronal. Again, I know some of these things, maybe like, there is no way they could ever teach you my exam. Until you see it, just do it on your exam. So please make sure you know the stuff. Please, this is extremely important. I mean, it sounds funny here, but it's not going to be very funny when you see it on your test. Okay, so, and remember, people that have low body dementia, they have this alpha-cinucline business with the brain. So just something you want to keep at the back of your mind as you study.

And then people that have frontal temporal dementia don't forget your big bodies. Your big bodies, your big, big, big bodies. Very, very important to know those for your test. All right, so we've talked about how to treat Alzheimer's dementia. We said that, oh, first line is an acetylcholesteroid inhibitor. Well, what can we use as second line? Well, second line, you can use this drug known as memantin. Memantin is a good second line agent for Alzheimer's. So how exactly does it work? Well, memantin pretty much is an NMG receptor antagonist, right? NMG receptor antagonist. So you may be wondering, why would an NMG receptor antagonist be helpful for dementia? Or here's the thing, here's the thing. There's this whole thing known as a glutamate excitotoxicity that kind of happens in the brain. You know, glutamate is a neurotransmitter that acts on NMG receptors. And as long as he's doing his job, you know, your neurons are going to work fine. Remember, it's an excitatory neurotransmitter. But the thing is sometimes, if glutamate works on that NMG receptor too hard, it can make those neurons get a little too excited. And when they get a little too excited, they can start dying. That phenomenon is known as glutamate excitotoxicity. We can save that off by giving an NMG receptor antagonist, like memantin, right? Like memantin. It pretty much saves your neurons from dying.

Now, one other thing I want to say about dementia, because I know many of you may think that this podcast is going to be all about dementia factoids. But no, you could not be more mistaken because the USML is again, they're not stupid. They know that many of you have memorized Alzheimer's. Hey, this. I'm a like plaques, neurofibrelaritangles. Blah, blah, blah, blah, blah, blah, blah, blah, blah. Don't get me wrong. Do they test those things? Yes. They do. But these days, especially since like last year, they've started testing more of these accessory concepts with dementia, right? Accessory concepts, right? So we're going to be reviewing all of those accessory concepts in addition to, you know, the high yield stuff. You should know about the actual dementia. Right? So what if they give you a question about a person that, again, struggling with activities of daily living, you know, has Alzheimer's, basically, and the person, you know, no longer wants to go to the senior citizen center. Does no one to interact with their kids anymore? The person's having issues with sleep, right? You know, the person is beginning to tell the physician that they don't feel like living anymore. What should you be thinking about? I really hope you're saying, ooh, divine. Sounds like this person has developed depression. Right? So the fact that a person is demented does nothing you should choke everything up to the dementia. Dementia can absolutely, positively be associated with depression.

And how do we treat depression in a demented patient? Pick the answer that talks about an SSRI. Pick the answer that talks about what? An SSRI, a selective serotonin reoptic inhibitor. Right? Now, one thing I especially want to say about dementia that's a side concept is this whole thing with dementia mimics. Right? So B12 deficiency on the USML Es and hypothyroidism actually can present as dementia. They can have a lot of dementia symptoms. Right? So that's why many times checking the B12 level and the TSH level is not necessarily a terrible idea when you're worried that a person may potentially have dementia. Right? And then whenever you see a person develop dementia like very suddenly like kind of out of the blue, you're like, whoa, within like two weeks, you just have this big cognitive impairment that just kind of perks up. Think of something like some kind of drug toxicity, right? Anticholinergic's not a good idea. Right? They can cause like the Lyraman, the dementia like symptoms. And then don't forget that also having like a subdural hematoma. You see a person, you know, all 70-odd grandpa that then suddenly starts losing his memory within like a week or whatever. Think of a subdural hematoma, you know, many times they will fall and then they'll get in trouble. Because remember, subdural hematoma is a slower bleed so they can live for longer. They can go a couple days, you know, before they start manifesting some crazy symptoms.

And again, remember, we tend to find that in people that are very old or people that are alcoholics, right? Because people that are old or people that are alcoholics, they are brain shrinks. They have cerebral atrophy. When you're brain atrophies, then it's not like your skull is going to atrophy with it, right? It's just your brain that's going to atrophy, right? Alcohol kind of shrinks your brain. So the thing that's going to happen is that you're going to have a cortex that is just slinging around in a fixed box. That's the skull. That can last rate your bridging veins and that can cause a subdural hematoma. You can get in big trouble when you're exempt, right? So don't forget those stains. Don't forget that anti-collinergics can cause these issues. Don't forget that subdural hematomas can cause these issues. And then another thing that can cause this acute dementia if you may is delirium, right? Delirium can present as dementia. Again, whenever you see things just arise very quickly just over days, you can just get dementia in days, right? Think of some kind of cause, you know, kind of bothering along these lines. Another one you'd like to throw an exam sometimes is especially a person who wants n-stage liver disease, hepatic insect fallopathy, that can cause this acute dementia if you may, right? So just going to keep that at the back of your mind as you're preparing for your exams, right? And one thing that I want to say, they love this.

What are some drugs that are heavily contraindicated in demented patients? See, one big one are anti-collinergics. Big one, anti-collinergics. Anti-collinergics are a terrible idea if a person has dementia disorder, right? Because again, we know that anti-collinergics can trigger delirium, they can trigger confusion. You give an anti-collinergic to a person that has a dementia syndrome. You're going to like really, really, really shake those people up. So just don't do it. Anti-collinergics are drugs with anti-collinergic properties like, you know, like a difid hydramine, for example, or, you know, you're tricyclic antidepressants and all those things. They're not a good idea in people that have a dementia syndrome. Another classic one are the anti-psychotics. The anti-psychotics are a terrible idea in people that have dementia, right? I don't want to do that because the thing is there's even black box warnings on these drugs that, hey, giving it to old people such people with dementia, it's not a good idea. And one of the dimensions that it's like really, really bad for are people that have like a Louis-Body dementia, right? People that have Louis-Body dementia, they're already in a state of dopamine deficiency. Do you think that blocking dopamine receptors is a good idea in those people? No, it's not. It's really not. It's really not a good idea, right?

In fact, they have an especially high risk of developing extra pyramidal symptoms as a result of those, especially like neuroleptic malignant syndrome. NMS is something that we really, really, really worry about when you give an anti-psychotic to a person that is demented, right? Especially people that have Louis-Body dementia, that's like the strong solid association. You want to know for your exams, right? That's the strong solid association. You want to know for your exams, right? Really, the only times that we give anti-psychotics to people that are demented is if they're like agitated or, you know, they're, you know, they're agitated. You can give them an atypical anti-psychotic. But a big no-no, please never, ever, ever gives something like aloperoidol. First, your ancient anti-psychotic to a person that's demented. That's a terrible idea. That is a terrible, terrible, terrible idea, right? Terrible, terrible, terrible idea. Honestly, if I were you, I would just refrain from anti-psychotics and Louis-Body dementia patients on your exams, right? So just be careful, just be careful, right? And again, what's the epidemiology behind dementia? What's the number one cause of dementia? Well, the most one cause of dementia is going to be Alzheimer's, right? Alzheimer's is the most one cause of dementia. Number two is going to be Louis-Body dementia, dementia of Louis-Body's. I believe back in the day, number two was Vascular dementia, but that has kind of changed.

These days, Louis-Body dementia is number two, and then number three is Vascular, Vascular dementia, Vascular, Vascular dementia, right? And then, you know, I know one kind of dementia many of you may have heard about is Parkinson's disease dementia, right? They really tested on the USML Es, but I'm just going to say a few things about it. Basically, Parkinson's disease dementia, you're going to see Tharise many, many years after the modal symptoms and Parkinson's. It's more like a late feature of Parkinson's. You know, versus Louis-Body dementia with the memory issues tend to be a pretty early feature of disease within the first few months of disease, you're having those dementia symptoms, right? So just going to keep that at the back of your mind, but people that have Parkinson's disease dementia long, long time after their modal symptoms start. That's when they have that Parkinson's disease dementia, right? Parkinson's disease dementia, right? And what if they give you a question about a patient? This patient is started on therapy for Alzheimer's. And then you're told that the patient, you know, they give you an EKG. And you notice that, man, this person, you know, some curious complexes are missing, and the PR interval is prolonged. And then they ask, what is the most likely mechanism behind the observed EKG findings? I would really hope you're picking the answer that talks about drug toxicity or colonergic excess, right?

Again, this is how our friends at the NBM Es can heavily integrate things on your exams, right? So remember, the way we treat Alzheimer's as I've said already is to give an acetylcholinesteris inhibitor, right? When you give these acetylcholinesteris inhibitors, they're going to bump up your levels of acetylcholine. When they do, it's almost like you're taking an organophosphated ascents, right? Although, a lot less potent than that, right? But you can have like a colonergic toxic trauma as a result of that, like, you know, like Brady Cardiolidin to a heart block. They can have like diarrhea. They can be peanut themselves, right? Because they're just, you know, rest and digest, right? You're going to be pain, pain, pain, pain, a lot, right? So please, uh, make sure you know that. Make sure you know that. Make sure you know that. And again, honestly, if you love the way I teach, you would love my classes even more, right? If you love the way I teach these podcasts, you'll love my classes even more. You know, I have a step one class starting today and then I have a bunch of others, you know, step one to step three classes, taking place later this month. And then I have this epic 50 hour step two, step three class that's taking place in the first two weeks of June. I'm telling you, these classes are very helpful and there's lots of integration. And you're just going to really, really understand the material, really, really understand the content.

I've had many people take my classes and they've done extremely well on their exam. So again, I will encourage you. Consider my classes. They're all held over Zoom. If you're interested, just shoot me an email through the website and I can give you some more information. All right. So let's keep going, right? So again, don't, don't be misguided on this whole thing with with colonergic toxic drums and acetylcholester is inhibitors and management of Alzheimer's. That's literally a very nice fancy because again, they know that all of you have memorized farmer with organic fat, fat, and it's not a bad name. So what do they do these days? Just find an unusual person that's getting an acetylcholester is inhibitor and then test colonergic toxic drums in them. Tested in an unsuspecting patient for a US Emily exam tinker, like a person that has Alzheimer's, for example. So keep that at the back of your mind. That's a very high-yield association to know for your exams. All right. Now, what if they give you a question about a person again that has, you know, the have a, you know, they tell you that, oh, this person for the past six months, they've had a lot of cognitive decline. And then they tell you that, you know, the person comes to the office is brought by their spouse or their kids or whatever. And that this person has, you know, like a mass, a lower abdominal mass on your exams, right? And they tell you that the person has like impaired gate.

If you see this, think of normal pressure hydrocephalus, right? Think of MPH, right? Waky wet and wobbly believe it or not. One of the ways we diagnose MPH is to look at your symptoms before we do a spinal tap and then look at your symptoms after we do a spinal tap. If you see a dramatic improvement in symptoms in these people, that's pretty confirmatory for normal pressure hydrocephalus, right? And again, as I've said, ventricular period to new shant is not a bad idea for management in these in these people, right? And then again, I've already talked about Louis body dementia already, right? But again, just remember the many different things they can test about Louis body dementia, right? You see a person that is demented and they have like Parkinsonian symptoms or they have constipation or they have orthostatic hypotension or they have visual hallucinations, right? These symptoms that are not there or they have a lot of falls or of syncopal episodes or sleep problems, really, really think about Louis body dementia. And since we're talking about this stuff, I just want to talk about the causes of visual hallucinations on the USML Es. When you see the term visual hallucinations, there is a pretty limited differential. You should be keeping at the back of your mind with your USMLE exams. Number one, think of Louis body dementia. And not since the most common cause, Louis body dementia is a cause of visual hallucinations on the USML Es.

Another classic cause of visual hallucinations on the USML Es is a person that has alcohol withdrawal. You know, many of us know this as alcoholic hallucinosis, right? Visual hallucinations, we can certainly find in a person that we're drawing from alcohol. And then a third cause of visual hallucinations on the exams is going to be a person that has delirium, acute delirium. Delirium has a very strong association with what with visual hallucinations on the USML Es? Very strong visual hallucinations on the USML Es, right? And then what if you see a person that has, you know, dementia and they're seeing things that are inappropriate or they pick up these obsessive compulsive behaviors like they start this workout program or this new diet program or whatever. You really want to think about frontal temporal dementia under those circumstances. You want to think about FTD, right? Pix disease under those circumstances, right? It has those kind of weird associations on the exams. And then if you see a person that has dementia and they have a lot of neuro deficits, right? So you notice that they have like, you know, like, and you notice that the neuro deficits are pretty localizable. You're like, wow, this person has like left-operated extremity weakness. It's like you can almost like pinpoint a vessel in the brain that is impaired or must have stroked for them to have this problem. You want to think about vascular dementia under those circumstances, right?

You know, they like to use this term stepwise declining neurologic function on the exams. Basically, you see a person that has all these like stroke symptoms and then you notice that in addition to that, they have a cognitive impairment. You want to think about vascular dementia on your exams, right? You want to think about vascular dementia on your exams, right? So one thing though, I want to say just be careful though. If you see a boy, I guess I was just a side point since I'm talking about it, you see a little child, it can be a boy or a girl. And this boy is having these like stroke-like symptoms that are episodic, right? And then you notice that the a bicarb is extremely low. Then you want to think about mitochondrial disorder, right? This is the encoder, me las. I believe me las means metabolic and cephalopathy with a lactic acidosis and stroke-like episodes, right? So you see stroke-like episodes, you see lactic acidosis, right? Think about a person that has a mitochondrial disorder like me las, M-E-L-E-S, right? And some of you may wonder, gee, why do they have a low bicarb? Well, it's because they have lactic acidosis. But again, an even better question, gee, divine. Why do they have the lactic acidosis? Well, it's a mitochondrial disorder. If you have mitochondrial problems, I don't know about you, but it sounds like you're going to have issues with energy production. Because remember, the mitochondria is like the powerhouse of a cell, right?

So if you mitochondria is not working, there's a lot of processes that are not going to go very well. You know, like, I don't know, like the electron transport chain that generates like a ridiculous number of ATP's. So what's going to be like your primary energy source? It's going to be glycolysis. What is the thing that shows up at the end of glycolysis? I don't know, lactic acid, right? So that lactic acidosis that we see in me las makes a lot of sense. Again, many things in life work better when you just try to understand, instead of just like blindly memorizing stuff, blindly memorizing stuff usually doesn't work out well for people. Or to be honest with you, it severely limits the kind of potential you can have with regards to exam scores. That's just the truth, right? That's just the truth. So just be careful on your test. All right, just be careful on your test. All right, so I'm just something I kind of figured I want to throw in. I'm just trying to think, is there any other thing about dementia that I've not talked about? You know, I said that in Alzheimer's, you have atrophy of the hippocampus. Also your temporal lobes, you know, your temporal lobes also atrophy in a person that has Alzheimer's. So you should probably know that for your exams. And you know, you see a person that has dementia that develops very rapidly, you know, out of the blue.

And then you notice that this person has, you know, he develops very rapidly and they have like increased deep tendon reflexes. They have like myoclonus, right? They probably want to be thinking about crates, felt, yeah, cold disease, right? CJD, they're going to have increased levels of this 1433 protein in their CSF, right? Increased levels of the 1433 protein in their in their CSF. So that's really know that if I were you. And then you see a person that you know was maybe like a sex worker years ago or an IV drug user. And then the person has like these neuro deficits severe cognitive impairment and their CD4 count is like 15. That person has HIV associated neurocognitive dysfunction, right? We call that hand these days, we call that hand these days, right? And then if you see a person that has a again low CD for account or you know like a post transplant patient. And the person has like dementia like symptoms and you notice that man, this person has white matter changes on brain imaging. Then I would really, really hope you're thinking about a person that has progressive multifocal look once a fallopathy, PML, right? Remember that tends to arise in people that immunocompromised from a GC virus reactivation. So again, I think I've kind of hit all the major major things I want to I want to discuss again, I really encourage you to listen to this podcast maybe like twice. You're going to see the stuff on your exams, you know, you're going to see it on your exams.

That's just a given. You're going to see it on all your USML Es, all your complex exams. You can pretty much never run away from dementia. That's just the truth. You can pretty much what never run away from dementia. And again, I have this podcast on Apple Google and Spotify. I've got a You Tube channel, divine intervention, USMLE podcast and videos where I post the videos and podcasts that I make. And then, you know, I have my 25 hours step one class starting today. And then all the classes offer for step one to step three. I have a 2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 I have a website called Divine Intervention Life Lessons.com. Many of you know I'm a Christian. So every week I post like 2 or 3 podcasts where from a biblical perspective, I address a life lesson. Believe it or not, I have like a wooden 330 podcasts on there as of today I think. Pretty sure I made a episode 3 31 yesterday. So you can check it out. There's actually a lot of podcasts associated with that called the Divine Intervention Life Lessons Podcast. So I think I'm going to go ahead and stop here.

This is probably one of my highest your podcasts I've ever made. Study the stuff. I know I use keeps here me say, study the stuff, learn the stuff, study the stuff, learn the stuff. It's going to be a bunch of questions on your exams. Easy points if you know what you're doing, right? And I feel like in this podcast I try to emphasize some of the stuff about dementia. You may not see it in the many other resources. Actually, I'm still being very, very high up for the US Emily exams. So thank you for listening to me today. I will see you in an episode I guess 600. Wow, that's a milestone. So this is 599 I believe. So I'm going to see an episode 600. Wow. So I have a wonderful day. I'll bless you and bye for now. Thank you.

Diabetes, hypertension, and hyperlipidemia.

MCI involves memory issues but preserved Activities of Daily Living (AD Ls); Dementia involves struggling with AD Ls or low MMSE scores.

Acetylcholinesterase inhibitors (e.g., donepezil, galantamine).

Frontotemporal dementia and Normal Pressure Hydrocephalus (NPH) (where a VP shunt is preferred).

Lewy Body Dementia, alcohol withdrawal (alcoholic hallucinosis), and acute delirium.

MELAS syndrome (Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like Episodes).

Amyloid plaques.

Neurofibrillary tangles (Tau protein).

Ventricleomegaly disproportionate to cortical atrophy.

They can trigger delirium and confusion by interfering with the already compromised cholinergic system.

Memantine; NMDA receptors (to prevent glutamate excitotoxicity).

Neuroleptic Malignant Syndrome (NMS), especially with typical agents like haloperidol.

Amyloid plaques.

Neurofibrillary tangles (Tau protein).

Ventricleomegaly disproportionate to cortical atrophy.

They can trigger delirium and confusion by interfering with the already compromised cholinergic system.

Memantine; NMDA receptors (to prevent glutamate excitotoxicity).

Neuroleptic Malignant Syndrome (NMS), especially with typical agents like haloperidol.