DIP Episode 336 - USMLE Step 2CK Rapid Review Series 64 (+8/25-28 Step 2CK/3 Course Reminder)

Okay, welcome. My name is Devine. This is episode 336 of the Divine Intervention Podcast. I'm going to be continuing our rapid review series for the US Emily Step 2 CK exam. Obviously this also applies to people taking the step 3 exam. Okay, so what if they give you a question about and again I guess one thing I should zero quick. If you're taking step 2 CK anytime soon or step 3 anytime soon let's say like the end of this month or early next month I know many people are trying to get their scores in time for ER As. I do have a review course. It starts with the NBME Testicking Strategies course. It's taking place tomorrow from 2 to 4 30 p.m. Pacific Standard Time. And then the review course for step 2 CK step 3 takes place Thursday Friday Saturday of this week from 8 to noon Pacific Standard Time. We'll take a one-hour break and then we'll go from 1 to 5 Pacific Standard Time. Again we're going to cover tons of subjects. Pied surgery I am Opie Guy, psych, neuro, ethics, bio stats, professionalism, communications, healthcare systems, multi-system processes and disorders. Again I've had many people that have taken the exam especially people that have taken the exam like very recently. I've actually found the course to be extremely helpful. I've heard I've got many emails from students that attended saying oh wow a lot of the things we discussed should up on my exam. So if you're interested just ship me an email through the website and I'll give you some more information.

So let's just jump right into it. So what if they give you a question about a 32-year-old female and they tell you that two years ago she had this episode of Blur revision for about two weeks that kind of resolved. And then since she's been completely fine but that now for the last two days she has been having like pin like pin in her right eye and that pin doesn't seem to be getting better. And then they ask you for your next best step in management. Well I'll really hope on MBM exams the very first thing you want to do is to get an MRI of the brain with IV contrast right because this person likely has optic neuritis. This person likely has optic neuritis. Remember optic neuritis is classically associated on MBM exams with multiple sclerosis right. So optic neuritis associated with multiple sclerosis you diagnose it by getting an MRI of the brain with IV contrast. This is actually an ophthalmologic emergency you need to treat you need to give an IV corticosteroid to fix the person's problem right so that they don't become permanently blind. And the thing is sometimes again many people have heard me recent podcasts say that the MBM is they've been doing this thing in recent times of using derivative answers. What in the world waiting by derivative answers? Derivative answers are answers where you're like oh you're reading the question you know exactly what it is and then you look at the answer choices and you're not seeing what you're looking for right.

So a classic answer they can do for optic neuritis with multiple sclerosis is they can call it unilateral afferent popularity defect okay. Unilateral afferent popularity defect. Because remember it's a problem with crinonor of two right that's what's called optic neuritis. Crinonor of two is the optic nerve right. So if you see a unilateral afferent popularity defect again an woman that seems to have these neurologic deficits that seem to come and go I really want you to think about optic neuritis associated with multiple sclerosis right. And again remember with trigoptic neuritis because optic neuritis is almost considered an exacerbation of a person's MS we're gonna treat those people with IV corticosteroids to cause immediate remittance of their symptoms. Now what if they give you a question about about a 42 year old female and they tell you that for the last you know six months she has started losing her way like she has started being very forgetful not able to find the supermarket not able to get back home and she's beginning to become more and more dependent on individuals as her you know for her activities of daily living and they ask you what's the most likely genetic disease this person has. I really hope you're seeing this person has Down syndrome right. It's person has Down syndrome. Membrane Down syndrome. These people they have trisomy 21 right so on chromosome 21 that's where you have the gene that codes for the amyloid precursor protein right.

So the thing is these people over time because they have like three doses of the protein product of the gene APP they basically develop a deposit a lot of amyloid plucks in their cortex right in their brains and those people ultimately end up getting in a lot of trouble with Alzheimer's. Many people I'll see the vast majority of people that have Down syndrome they're gonna get Alzheimer's around the age of 40 right so that's something that's I owed to keep in mind for for exams.

Remember when people have Alzheimer's the way we're gonna treat them is we're gonna give them something that's gonna boost their levels of acetylcholine because remember in Alzheimer's disease you essentially have a loss right you essentially have a loss of the basal nucleus of minor the basal nucleus of minor the basal nucleus of minor is the part of the brain that produces acetylcholine so if that part of the brain is destroyed you will not be able to make acetylcholine and that's what part of the thing that explains the pathophysiology behind Alzheimer's disease so we're gonna treat Alzheimer's disease by doing something that will boost acetylcholine levels we're gonna use a drug like Dunepezil galantamine or River Stigmin right these are all acetylcholine esteries inhibitors that have been approved for use in the treatment of Alzheimer's right so those are acetylcholine esteries inhibitors for Alzheimer's again you can not just use any acetylcholine esteries inhibitor you want right in fact since I'm talking about acetylcholine esteries inhibitors let's just kind of hit on a few key ones that they love to test on exams right so we just said that for Alzheimer's the acetylcholine esteries inhibitors that are approved are Dunepezil galantamine and River Stigmin right they boost up your levels of acetylcholine and you use those to treat Alzheimer's disease although they just maybe help you a few months or whatever the Alzheimer's release is essentially a terminal illness right and then the second group of acetylcholine esteries inhibitors I'll talk about once you think of pyridolstigmin right remember pyridolstigmin is the drug that we used to get rid of the symptoms of myestinia gravis because remember in myestinia gravis the thing that happens is that these people right they formed autoantibodies against the nicotinic acetylcholine receptor when you make autoantibo

dies against the nicotinic acetylcholine receptor then your basically going to destroy those receptors so you're not gonna be able to respond to acetylcholine right so the thing that happens is that we give an acetylcholine esteries inhibitor like pyridolstigmin that will bump up the levels of acetylcholine and those acetylcholine molecules will outcompete those nasty antibodies on the surfaces of the nicotinic acetylcholine receptor and other acetylcholine esteries inhibitor we use on MDM exams is phyzostigmin right remember we use phyzostigmin in settings of atropine overdose we use them in settings of atropine overdose because remember atropine the way it works is that it's a most macrownic receptor antagonist so when you block those most macrownic receptors you're going to get an anticholinergic toxic room you're gonna get things like things like tachycardia you're gonna get things like my dry asses right those people are gonna be really hot so they're gonna have like a fever on MDM exams but it's it's a non-infectious fever right they're gonna get a fever that is non-infectious on MDM exams so how do we treat it where we're gonna give an acetylcholine esteries inhibitor like phyzostigmin right like phyzostigmin your your fix and atropine overdose with phyzostigmin right so phyzostigmin is at acetylcholine esteries inhibitor when you inhibitor acetylcholine esteries and levels of acetylcholine are gonna go up and if you acetylcholine levels go up right that's going to outcompete that atropine that's on the surface of your of your macrownic acetylcholine receptors remember though on the flip side we use atropine right to treat organophosphate poisoning because organophosphate poisoning is almost like the reverse condition right organophosphates they are very good acetylcholine esteries inhibitors right so because they are acetylcholine esteries inhibitors right the

y're going to boost your levels of acetylcholine right and that's gonna cause that colonergic toxidrom so the president has a colonergic toxidrom it would make sense that you want to reverse that toxidrom by giving an acetylcholine receptor antagonist like atropine remember you're gonna give atropine first the first thing you always do is to give atropine after that you're gonna give prelydoxine right prelydoxine will help you regenerate the acetylcholine esteries that has been inhibited or basically crucified by by the organophosphate okay and then remember a nile stigma is another classic acetylcholine esteries inhibitor emission on an exam basically the way nile stigma works is that we use it generally for both the half-states of ilius right so let's say a person has just come out from surgery they've just had an asthesia remember an asthesia basically grinds your GI tract at a ton of opioids right so it's gonna grind your GI tract to a halt if you grind the president's GI tract to a halt that's going to cause ilius right so they're gonna have like a functional bowel obstruction so the way you're gonna fix that problem right is you're essentially gonna give nile stigma right when you give nile stigma in inhibitor acetylcholine esteries that bump up their levels of acetylcholine and that's gonna cause GI motility right that's gonna cause GI motility that's gonna cause GI motility and that's gonna release that ilius and remember we can also use nile stigma in the treatment of overflow in continents right we can use nile stigma in the treatment of overflow in continents because remember in people that have overflow in continents classically those people on NBM exams they're going to have a very high post-void residual volume right you'll have a post-void residual volume of like 300 400 500 milliliters right so the thing is those people's detrusor muscles do not sense

that the bladder is full so the thing we're gonna try to do for those people is we're going to try to make those detrusor muscles contract and the thing that makes those detrusor muscles contract is acetylcholine so if we're given acetylcholine esteries in inhibitor like in your steaming that's gonna bump up the levels of acetylcholine that's gonna stimulate those detrusor muscles and the president's gonna be able to pee although remember you can also use Bethany call or Carbacol right those are most chronic receptor agonists you can use those as well for the treatment of overflow in continents and remember overflow in continents you can also try like intermittent catheterization to get that urine out of those people's bladder okay so that's very high yield to know for for exams now what if they give you a question about an archaeologist right they tell you that you know he studies like agent animals like like old fossils and then they tell you that over the last three months he has become increasingly forgetful right and he has like these he has myoclonus right sometimes instead of telling you the word myoclonus on an in-beaming exam they'll describe it to you they'll tell you that he has been having these rhythmic jerk-like movement of his of his extremities right whenever he's stuff like that whenever he's here rapidly progressive dementia we're pressing goals from normal to demanted within like a few weeks to like a few months at best and want you to think of Kreutzfeld-Jakob disease don't you think of Kreutzfeld-Jakob disease Kreutzfeld-Jakob disease remember it's spelled as C-R-E-U-T-Z-F-E-L-D-T Kreutzfeld and then Jakob is J-A-K-O-B right disease right it's a pre-on disease right remember these people if you were to perform a longer pointer on them and you check their CSF you're gonna find increased levels of the 1433 protein right you're gonna find increased l

evels of the 1433 protein there's no treatment for CJD for present-guest CJD they're going to die and one thing I want to say that's very high-old on in-beaming exams is that having CJD is a contra indication to get in a transplant right because these people they're gonna die regardless so why give them a transplant so CJD patients do not get transplants on in-beaming exams that's very high-old to know again I know some of the things that may be seeing here maybe like I don't know if they will test that think again trust me I work with thousands of people right that I've taken this exam right I know exactly what I'm talking about here right now what if they give you a question about a patient and they tell you that oh this patient has a family history of chronicly red disease and that over the last you know four to six weeks this patient has been having so many neuropsychiatric symptoms right like he has been having like his speeches dominated by like loose associations he's saying all this weird stuff right he's he keeps to himself he stopped attending classes and stuff like that if you see something like this I really really want you to think about well-sense disease right I really really want you to think about well-sense disease remember well-sense disease is a copper is a copper excess a problem right usually that raises from an ATP 7b that's very high-old to know ATP 7b gene mutation right so the thing is many times that excess copper can go and deposit in the basal ganglia now when it deposits in the basal ganglia those people begin to have movement the soldiers so they can have Parkinson's like features right they can have neuropsych symptoms many times they tend to almost have like a schizophrenia like presentation on MDM exams now remember if a woman has well-sense disease what kind of contraceptive option should not be available to her and hope you're seein

g the copper IUD right remember the copper IUD is something that you absolutely absolutely should never give to a person that has well-sense disease remember the copper IUD also avoided in people that have like breakthrough you're in bleeding right so in general right well-sense disease they have a copper excess so you have absolutely no business giving those people a copper IUD right and remember usually these people when you the diagnostic test is to check the levels of seroloplasmin right to check the levels of seroloplasmin right the levels of seroloplasmin will be low in these people that have well-sense disease okay you'll be low in these people that have well-sense disease now what if they give you a question about a child right she's a five-year-old girl they tell you that she has no history of intellectual disability they tell you that at birth her abgascourt were eight and nine one and five minutes respectively and then they tell you that this girl that she her parents were called into school because she doesn't appear to be been attention in class right she always seems to stare staring to space during class whenever you see stuff like this right I want you think about abson seizures right this person has abson seizures this person has abson seizures now it's very high you'll remember that on mbm exams abson seizures are a kind of generalized seizure right so again you may be reading an abson seizure question and the mbm in the great kindness they will not put abson seizures and answer they'll put generalized seizures and answer if you see that that's totally fine obviously they put abson seizure that should be what you should go for first right but if you don't see that as an answer it's not a bad idea at all to pick the answer that says generalized seizure you'll be correct doing that now remember when a person has an abson seizure what are you going to f

ind on EEG remember you're going to find that three hurts or three per second remember the frequency measure right so three hurts or three per second spike and slow wave pattern you're going to see that on an EEG right again you don't need to know exactly what that looks like we need to know that buzzword right so how do we treat abson seizures remember we're going to treat abson seizures with ifo-soxamide again this is another classic classic classic classic thing that our friends at the mbm is instead of putting ifo-soxamide as an answer they'll put the derivative answer which is the drug mechanism of action remember ifo-soxamide works by being a tea type calcium channel blocker right ifo-soxamide is a tea type calcium channel blocker it's a tea type calcium channel blocker that can be used in the treatment of abson seizures right and again the thing is the mbm is occasionally they've actually written a few questions where they try to like really make this kind of question hard right so they'll give you an abson seizure question and instead of giving you that oh it should ifo-soxamide they'll actually put multiple types of calcium channel blockers as answer choices right so they can put like L type calcium channel blocker tea type calcium channel blocker P type calcium channel blocker again remember the tea in ifo-soxamide for the tea in tea type calcium channel blocker okay for the tea in tea type a calcium channel blocker now what is the most common cause on mbm exams of a central retinol vein occlusion what is the most common cause on mbm exams of a central retinol vein occlusion i really hope you're saying oh divine i'm thinking more along the lines of polycythemia vera right remember polycythemia vera tends to cause central retinol vein occlusions on mbm exams okay it tends to cause central retinol vein occlusions on mbm exams remember those people you will not

find because unlike central retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol ret retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retinol retin I figured out all the emails I was getting from people that were getting benefit from those from those life lessons I figured out just go ahead and make a new website so you can even find it on Apple Podcasts called the Divine Intervention Life Lessons.

So thank you for listening I'll see you next time God bless you. Thank you.

3 Hz spike and slow wave pattern (or generalized seizure activity).

Polycythemia vera.

Acetylcholinesterase inhibitors (e.g., Pyridostigmine).

Increased levels of 14-3-3 protein.

Acetylcholine, due to damage in the basal forebrain.

Receiving a transplant (due to high mortality rate).

Pyridostigmine (an acetylcholinesterase inhibitor).

It is an acetylcholinesterase inhibitor that increases A Ch, allowing it to outcompete the muscarinic receptor antagonist (atropine).

Wilson's disease.

T-type calcium channel blocker.

Donepezil, Galantamine, or Rivastigmine.

1) Atropine (muscarinic antagonist); 2) Pralidoxime (reactivates A ChE).

Pyridostigmine (an acetylcholinesterase inhibitor).

It is an acetylcholinesterase inhibitor that increases A Ch, allowing it to outcompete the muscarinic receptor antagonist (atropine).

Wilson's disease.

T-type calcium channel blocker.

Donepezil, Galantamine, or Rivastigmine.

1) Atropine (muscarinic antagonist); 2) Pralidoxime (reactivates A ChE).