DIP Episode 175 - USMLE Step 2CK Rapid Review Series 23 (Psych)

Okay, welcome. My name is Divine. I'm a resident. This is episode 175 of the Divine Intervention Podcasts. And in this podcast I'll be continuing my rapid review series for the USM list of two CK exam with a focus on psychiatry. This will be series 23. So let's begin. What if you get a question about a patient that has been vomiting, like has a like a BMI of 16. She's a cheerleader. She's been vomiting, throwing up. You know, she's hypotensive. She's more dynamicly unstable. And the ask for your next best step in management. All that beyond an exam. I would hope you're seeing to admit that patient to the hospital. In fact, if you need to do it involuntarily, that's absolutely fine. So this patient has anorexia nervosa, right? So remember anorexia nervosa? Those people have a distorted image of their bodies, right? So they think that they're too heavy, even if they have a pretty low weight. And the classic thing you want to keep at the back of your mind for purposes of the MBM exam is that when people have anorexia, their body weight has to be below normal. So those people have to be under weight, okay? If a person is normal weight or overweight, they cannot have an orexia nervosa on an MBM exam. So in this case, this person has like a BMI of 17. That's definitely in the under-width category. So this person for sure has an orexia nervosa. And you want to be able to compare and contrast anorexia nervosa with bulimia, with binge eating disorder.

Anorexia nervosa, basically again, the person you know has all these like a maladaptive images of their bodies, right? So they work out a ton of vomit and all that stuff to lose weight and they are less than normal weight. If you see a person that essentially does the same thing. So again, they may binge, they may purge, they may work out the ton to lose some weight, right? But they have like normal weight of their overweight, then that's bulimia, okay? So if a person binges and then has a compensatory behavior associated with the binges, that's bulimia nervosa and by definition, a person that has bulimia on an MBM exam, almost either be normal weight or overweight. Now contrast that would binge eating disorder. This is something that tends to confuse people a lot on the USMLE exams. But when people have binged eating disorder, they binge, but actually they don't have compensatory behaviors like the people that have bulimia. So they don't purge, they don't work out nothing, they just binge and just feel guilty about their binging. Okay, if you see that, think about binge eating disorder. So it's the absence of the compensatory behavior that separates binge eating disorder from bulimia nervosa. And then the presence of a normal weight or being overweight is what separates bulimia nervosa from an aurexia nervosa. These are very high-y old key differences to keep at the back of your mind, for exams.

Now, what if you get a question about a person with an aurexia nervosa and they ask you about the electrolyte abnormalities? Well think about it, this person, let's say they've likely been throwing up a ton, right? So they may even have dental caries from that. But another thing you may see in that circumstances, because they throw up a lot, they become hypochloremic, right? So they become hypochloremic and they also become hypochloremic. They are hypochloremic because they are losing a lot of electrolyte rich fluid. And some people may say, but wait, divine, these people are volume down. Why are they hypochloremic? The thing is, almost always, whenever a person is volume down, being volume down typically, believe it or not, is almost always associated with hypochloremic, namely, the exact same. The only exceptions to that room, where a person will be volume down and be hyper-metremic, is when the person has some kind of diabetes insipidus. It has central diabetes insipidus, or nephrogenic diabetes insipidus. But you better believe it, as long as your ADHD mechanism is intact, as long as your ADHD mechanism is intact, volume depletion is almost always associated with hypochloremic on NBM exams. So this patient will be hypochloremic, right? And again, because they have volume down, now we increase the activity of the renein and jotencin ourosterone system. So our dosturone will waste a lot of potassium in the ayurine, so they'll be hypochylemic.

And remember that there's the alpha-intercalated cell that you find in the distal nephron. The activity of that alpha-intercalated cell is increased by our dosturone. So because you're dumping a ton of protons in the ayurine, those people have a metabolic alkalosis. So in general, if a person is vomitting a ton, they'll be hypochylemic, hypochloremic, and they'll have a metabolic alkalosis. These are all high-yield things to keep in mind. And I mean, anorexia nervosa, you know, again, like I said, you bring them into the hospital. If they have like depression, you may want to consider putting them on a drug like merthazapine. Okay? Merthazapine is an alpha, is an alpha-2 antagonist. Okay? That is used to treat depression with its associated with sedition and weed gain. So it may not be a bad idea in a person that has anorexia nervosa. Now, what if they give you a question about a patient, do you know that comes into the emergency room? And this patient has a profoundly decreased, I mean, profoundly elevated blood pressure. This is blood pressure is like 210 over 120. And then they tell you that this person has a population of my dry asses. What's your diagnosis on these circumstances? Well, I'll really hope you're thinking about some kind of cocaine overdose. Okay? Unlike cocaine intoxication, remember, cocaine is a sympathomimetic, right? So you have alpha-1 agonism. So that will increase systemic vascular resistance and raise blood pressure.

In addition, cocaine by being a sympathomimetic, you have population of my dry asses, right? So you have population of dilation. So what would your next step in management be here on an MBA mexia? Well, the thing you certainly do not want to do is to give a bit of blocker, right? Because remember, you don't want the on-opposed alpha stimulation, alpha-1 stimulation. So the thing you don't have those circumstances is you can actually give a benzodiazepine. That's an option that's tenable on an MBA mexia. Another thing you can consider is to give an alpha-beda blocker like her video law. I mean, sorry, like a little bit on law. That's something to consider. And then the fifth thing you could also consider on an MBA mexia is to give an alpha-1 antagonist like femtolamine. Those are all acceptable options for treating the hypertensive crisis associated with cocaine intoxication. And if you want to drop parallel to other things you miss on an MBA mexia, for a person has like a hypertensive crisis from tyramine and a monamine oxidize inhibitor, right? So remember your M.U.I. is like phenolcine, trineocypromine and isocarboxazid. You can treat those hypertensive crises with the drugs I just mentioned. Well, a benzodiazepine is probably not included on that list for a hypertensive crisis in the setting of a tyramine, whatever, with taking an M.U.I. And one thing that you could do to you on an MBA mexia is instead of giving you the classic M.U.I.

that people are used to, they may give you a question about a patient that has a history of Parkinson's disease that is being treated with a certain medication. And then they go out and consume like cheese or wine or crabs. And then they have like a hypertensive crisis. Think about the M.A.O.B. inhibitor okay? So the M.A.O.B inhibitors like cellulogen or arsagelline, those can also condasse certain circumstances trigger the hypertensive crisis that we see with the regular M.A.O.I.s. And then if they wanted to be especially devious on an M.B.A. mexia, one very nifty thing they could actually do is to give you a question about a patient on a leineasolid, right? Remember leineasolid actually has weak monamine oxidize inhibition activity. So it could potentially trigger hypertensive crisis again under the right circumstances. Although the right, the most likely thing they would do with leineasolid is to talk about a patient, you know, having like a MRSA infection. And then you're treating that person with leineasolid. And the person also has a history of depression that's treated with an SSRI. Well, because both agents are pro-cerotoneurgic, the contriger-cerotoning syndrome in the patient. So the patient will have like fevers, they'll have myoclonus, they'll have hyperreflexia. Now, one common problem that tends to pop up for people on MDMA exams is being able to differentiate cocaine intoxication from methamphetamine intoxication.

Because both agents are synpathomymetics, right? So cocaine will cause elevated blood pressures. The thing is one difference there with methamphetamine is that meth may cause slightly elevated. Well, you know, like basically the blood pressures will not be markedly elevated if you're dealing with meth. That's one. The thing is both cocaine and methamphetamine, both cospopulary mitriases. However, some unique features of methamphetamine intoxication that you want to keep at the back of your mind for exams is that meth is associated with poor dental hygiene. That's one. And then another one you may also see on an exam is the presence of prominent hallucinations. If a person has permanent hallucinations, you absolutely want to think about some kind of methamphetamine intoxication. And then what if they give you a question about like a 70 year old guy and this guy has a history of Parkinson's and they tell you that you know he's sent his Parkinsonian symptoms have gotten worse. So you bumped his dose of his Parkinson's met. It can be many different things like it could be that your bumped his carbidopalivo dopa. It could be that your bumped his rupeanyral. It could be that your bumped his hamantadine. It could be that your bumped his selegeraline racagelin. It can literally be any side. I mean any Parkinson's drug and taca pun, taca pun. Those are your contain inhibitors. Like basically if you bump any person's Parkinson's drug, remember those are pro dopaminergic agents.

Well think about it. How do we treat Parkinson's disease in general? Well we treat Parkinson's disease. I mean sorry how do we treat schizophrenia in general? We treat schizophrenia right by giving anti-psychotics and the vast majority of these anti-psychotics work by being dopamine receptor antagonists. So if you're treating a person for Parkinson's and you're giving them something that is pro dopaminergic, you can already begin to see that these people may have psychosis on the other right circumstances. So the thing is a classic and being an example question is to ask what is your next best step in management on the those circumstances? Well the first thing you want to do is try to lure the dose of the drug. Okay? That is your first step in management. You try to lure the dose of the drug. If the patient cannot tolerate that dose reduction, you put them back on the dose that control the symptoms. But the thing you want to do on that those circumstances is to add a drug known as quethyapine. Okay? Quethyapine. Remember quethyapine is one of those etypical anti-psychotics that has the unique side effect of cataracts. Okay? There's a nice way to remember that like cataracts, it sends on awful lot like cataracts, which will help you to remember that quethyapine is the inciting agent on the dose circumstances.

Now one thing I think I've mentioned this in multiple podcasts, but it always bears repetition because people seem to get this wrong quite pervissively on imbim exams is knowing what adjustment disorder is. Right? Many people seem to get adjustment disorder questions wrong for whatever bizarre reason, but here's the deal. Do we have adjustment disorder presences as a diet? Right? You'd almost always have these two things for an adjustment disorder question. The first one is that they will give you a lot of symptoms that almost seem to be like major depressive disorder style symptoms or generalize anxiety disorder style symptoms. But the thing is if you read the entire question, the things they give you will not meet the criteria. Is it that you have the number of symptoms you need and the timeline doesn't work out? So let's say the person may be sad, have low energy, and all that, whatever, but they've been having those symptoms for five days. Okay? So the timeline doesn't fit. So if you see something that is almost like major depressive disorder light or like generalize anxiety disorder light. Right? That's the first part. The second part is the presence of a recent stressor. Broke up with boyfriend. Broke up with girlfriend. Receive the recent like bad news or something of that sort.

If you ever see any of those things, a recent stressor plus MDD symptoms or generalize anxiety disorder symptoms that don't meet the full criteria for those diagnoses, your answer should be adjustment disorder on an imbim exam. That really is the classic presentation on tests. Now what if they give you a question about a patient that was in the military? And let's see his entire unit the past the way when he was on a tour in like some foreign country fighting the war. And then this person comes back to the US. And when this person comes back, this person is having a lot of nightmares, having a lot of flashbacks. And then they tell you that you are trying to interview this patient and this patient is answering questions in monosylobolts, has an expressionless face and is not really willing to share much in the way of information. And let's say this has been going on for the last two weeks or what your diagnosis. I hope you're telling me acute stress disorder. Right? Remember, a acute stress disorder occurs when a person has PTSD symptoms for less than a month. Okay? So that's classic acute stress disorder. There'll be a person that again has had some traumatic event. Maybe like usually, classically, it's a person in that like, you know, that was in the military that experienced a traumatic event well in the military. Or it can be someone that experienced like a major like vehicle accident, just something terrible, like a physical but terrible accident.

And then this that having flashbacks, nightmares, problems, sharing information about the event. If you see that and the symptoms have been going on for less than a month, think about acute stress disorder. If the symptoms have been going on for more than a month, think about PTSD. So my follow question here will be what's the first line medication for the management of PTSD? The first line medication is actually an SSRI, okay? But one thing that your friends at the MBME occasionally do to you is to ask you for the drug that is used to treat like the nightmares that's associated with PTSD. Do not pick an SSRI under those circumstances. Make sure you pick Prasosin, okay? Prasosin is the drug of choice for treating the nightmares that are associated with PTSD. Remember the P in Prasosin for the P in PTSD and that will help you keep that straight. Now what if they give you a question about like a 22 year old guy? This guy, he tells you that he has these sorting episodes where he becomes tremulous, he begins to sweat profusely, he can kind of dries up and he feels like he's losing control. And he tells you that he has had this thing multiple times over the last couple of weeks to month. What's your diagnosis? Well, I hope you're saying panic disorder, okay? I hope you're saying panic disorder. Remember a panic attack is when you have one such episode.

What if you're having a recurrence of those episodes and then you begin to be afraid, you begin to fear that, oh, I don't know if this episode will come again, then the person is essentially dealing with a panic disorder, okay? Panic disorder. And the first line of medication for the management of panic disorder on MBME exams is actually an SSRI. So again, that's something high you'd want to keep at the back of your mind. Now one thing I think I should go ahead and mention here that again, I feel like he's not emphasized the many resources is your friends at the MBME can give you a question about a patient where clearly the person has bipolar disorder, okay? The person clearly has bipolar disorder, but they will then choose to spend the bulk, like the bulk of the question describing the patient's manic symptoms and then you ask you for the next best step in management. The thing is if a person has bipolar disorder and they're acutely manic, giving a mood stabilizer as your first step in management is not a wise choice, because the thing is those mood stabilizers like lithium or like lamotrigin or things like that, it takes them a while to kick in, right? It takes them a while to kick in. So under those circumstances, the first thing you want to do is to administer an anti-psychotic. An anti-psychotic is the drug of choice for treating a patient that has acute mania. Notice my use of the term acute mania. That's again a very high-yield thing to keep in mind.

Now one other unusual way to test this construct is they can give you the same question and you know talk about a patient that you know has a histro bipolar disorder that was maybe diagnosed like six or seven weeks ago and then they tell you that the patient has been on lithium and then they tell you that oh with the patient being on lithium you've noticed that you know his symptoms are still poorly controlled and then they ask for your next step in management. Well the thing you really do want to think about under those circumstances is to actually consider adding an anti-psychotic as well to that person's medication regimen. Typically you add an atypical anti-psychotic. So if lithium is not cutting it for a person's bipolar disorder symptoms, consider adding lithium, I mean sorry consider adding an anti-psychotic especially an atypical anti-psychotic to obtain control of the patient's symptoms. Now remember your key side effects with lithium, right? Lithium can cause tremors, right? Lithium can cause hypothyroidism, right? And remember that lithium can also cause any effigining diabetes in sypedus and that effigining GI can be treated by the administration of amylo-right or triumtering which are in echannel blockers. They are a subset of the potassium sparing diuretics. Now let's go through some quick neurotransmitters, right?

So what if they give you a question about a patient and this patient has a histro trisomy 21 and this patient at the age of 41 this patient is beginning to forget their way home from the supermarket they are forgetting to turn off the stove. This call like a 15 out of 30 on a mini-mental status exam. What is the neurotransmitter that is low in this patient? These people actually have low levels of acetylcholine, right? So remember that these people have Alzheimer's, right? Remember having a histro down syndrome places a person at very high risk for early onset Alzheimer's. And so this person has Alzheimer's and in Alzheimer's in general those people tend to have low levels of acetylcholine. Remember that in Alzheimer's there are some key neuro anatomical associations that the mbim expects you to know for exams. So things like destruction of the bison nucleus of minor. Remember that's where acetylcholine is produced in the brain. So the person has destruction of the bison nucleus of minor. Then they would not be able to produce acetylcholine and then they will have signs and symptoms of Alzheimer's. Another thing that can also cause signs and symptoms of Alzheimer's is if a person has a deficiency of the enzyme chat, colina-sidyl transferase, colina-sidyl transferase is the retinitine enzyme in acetylcholine synthesis. So if you have an inactivity mutation in that that can also cause Alzheimer's.

Although another unique way they can test chat deficiency is they can test it in the context of something known as a congenital myostenic syndrome. They can test it in the context of something known as a congenital myostenic syndrome. Essentially the person will have a myostenic, a myostenic gravis-like presentation, but the asymptoms will not improve with the administration of an acetylcholine esterase inhibitor like a drifonia. Because remember if a person has good like regular myostenic gravis, well in myostenic gravis you make autoantibodies against the nicotinic acetylcholine receptor that you find at the level of the neuromuscular junction. And one way you can treat Parkinson's or even diagnosed Parkinson's. So let's say although these days everyone checks for the anti acetylcholine receptor antibodies, that's the diagnostic test of choice. But occasionally you may see this on exams where they say that oh they give you like the tensilent test. Remember the tensilent test involves the use of a compound known as a drifonium. A drifonium is a very short actin acetylcholine esterase inhibitor. So when it inhibits acetylcholine esterase, your levels of acetylcholine will go up at the synapse and that will outcompose those nasty antibodies and that will transiently improve the patient's symptoms. On the other hand, if a person has congenital myostenic syndrome where they have like a chats deficiency, they are not able to make acetylcholine in the first place.

So there's no acetylcholine in any way shape or form that hangs around the synapse. So if you were to give those people an acetylcholine esterase inhibitor like adryphonium because there's just no acetylcholine being produced. There's no acetylcholine levels that would increase to our compitose nasty antibodies. So a very nifty way they can test a choline acetylcholine transfer is deficiency on your exam. Maybe to give you a question about a patient that has a myostenic, myostenia-gravis-like presentation that feels to respond to the administration of an acetylcholine esterase inhibitor like adryphonium. That's a very high piece of information that you want to lock down in your mind for purposes of the USMLA exams. Now what if they give you a question about a patient that has like cogueurogenicity, has a white gate, is a um, bradykinetic? What neuro-transmitter is loing this disorder? I hope you're telling me this person has Parkinson's, remember Parkinson's is associated with low levels of dopamine. Okay? And what is a low-body dimension? What your transmitter is low? In low-body dimension? Outup, you also say low dopamine, okay? Low-body dimension has many, like many links to Parkinson's disease, although some weird things that they love to test is low-body dimension, for example, tends to be associated with visual hallucinations and syncopal episodes, right?

And the thing is in low-body dimension, those people tend to have dementia before they develop Parkinsonian-like symptoms, versus people with Parkinson's disease that tend to develop Parkinsonian symptoms first before the dementia sort of sets in. So those are all high-eal things to know. Now what if they give you a question about a patient that um, you know, is being treated with nine months of isoniasid for leshan, tibian, then the patients that's having seizures. Obviously, what caused this person seizures in the first place? Well, I hope you're telling me that the person got the seizures because they have elevated levels of GABA, I mean, sorry, of glutamate and low levels of GABA, right? Because remember, if you're taking isoniasid, you're supposed to take vitamin B6. Another name for vitamin B6 is pyrodoxyl phosphate. The thing is, if you don't take vitamin B6, then you have decreased the activity of the enzyme known as glutamate decarboxylis. And if you have decreased the activity of glutamate decarboxylis, you have a lot of trouble converting glutamates to GABA. So your glutamate levels will go up and your GABA levels will come down and that can predispose the patients to seizures. That can predispose the patient to seizures. So the person is seizing on an NBN exam, do not forget that you have high levels of glutamate typically and low levels of GABA. High levels of glutamate and low levels of GABA.

And I mean, obviously, if a person has serotonin syndrome, the levels of serotonin will be, you know, will be pretty high, right? And remember that your first test, if you suspect serotonin syndrome in a patient, is to measure the levels of 5 HIEA in the year. And remember, another name for 5 HIEA is, I believe, 5 hydroxyendol acidic acid, okay? Those are all key things to keep in mind. And then, obviously, if you get a question about a patient that is depressed, right? The levels of serotonin, the levels of meripinephrine, the levels of dopamine are all decreased on an NBN exam. And then if a person has a field chromosome tumor, right? What is the neurotransmitter that it's elevated? Well, I hope you're telling me that, again, the half-high levels of like caretellumins. And again, if you check their urine, you see elevated levels of caretellumine break-product, breakdown products like bedanefrains, things of that nature. And then, if they give you a question about a patient that has haunting tints, right? Remember, again, haunting tints, or the zomodominant inheritance, trial and fluid type repeats chromosome 4, people in your 40s, right? And remember that in haunting tints, actually, these people tend to have low levels of GABA and low levels of acetylcholine, but they actually tend to have pretty high levels of dopamine.

So that is why, typically, when a person is being treated for haunting tints, at least in early-stage haunting tints, you can consider treatment with drugs like tetrabenazine, tetrabenazine essentially inhibits the packaging of dopamine into vesicles. So tetrabenazine, or you can even use just a straight-up anti-psychotic, like haloparydon, for example. So again, these are all key things you want to keep at the back of your mind, for example. So again, haunting tints, low GABA and acetylcholine, and high dopamine. So I think this is where I'm going to go ahead and stop with this. As I do at the end of every podcast, I often want to want to learn from any exams. Step one, two CK, two CS, and step three. And they have pretty clinical medical exams, 30-ish off exams. And then I also do this thing where I do longitudinal tutoring, where if you're first, second or 30-year medical student, I tutor you for your shelf exams, your block exams, but at the same time, I tutor you for your upcoming USML exams. So I teach you content, and I teach you test-dicking strategy. And then I also offer this USML booster course. It's 10 hours for step two, CK and step three, and 20 hours for step one, where I, it's something that's ideal for a person that's at the end of their dedicated period, or feels good about your knowledge base.

If you want, like in a short period of time, to review the high yields with someone that can integrate many pieces of information for you together, and essentially go over things that are high yields and most knows for the USML exams. Feel free to reach out to me through the website, or you send me an email at divineinterventionpodcasts with an SAD end at gmail.com. And then I also offer tutoring for like general chemistry, organic chemistry, physics, biochemistry, histology and physiology. So if you have a college body that needs those, I feel free to reach out to me. And then if you're a med student applying to residency, so like an ERAS application, or a college student applying to med school, so an Anka application, I go for like one-on-one advising, coaching, tutoring, editing applications, personal statements, mock interviews, rec letters. I go for those things. Again, I've been in the admissions committee of a top two med school for more than a year. So I have a lot of experience going through this process and reading thousands of high quality applications. And again, I've worked with tons of people throughout these processes. And again, the vast majority of them have been overwhelmingly successful. And then finally, if you have like a medicine resident buddy that needs tutoring for the internal medicine training exam, or the internal medicine EBI and board exams, I do offer one-on-one tutoring for that as well. So have a wonderful rest of your day. God bless you.

I'll see you next time. Thank you.

Bulimia involves compensatory behaviors (purging, excessive exercise) following a binge; BED does not include these compensatory behaviors.

Hypochloremia and metabolic alkalosis. This occurs due to loss of chloride-rich gastric fluid.

ASD symptoms last for less than one month following a trauma; PTSD symptoms persist for more than one month.

Prazosin. Remember the mnemonic: 'P' in Prazosin for 'P' in PTSD.

Dopamine.

It suggests that the neuromuscular junction is being affected by autoantibodies against nicotinic acetylcholine receptors, confirming the diagnosis.

High glutamate and low GABA levels (due to decreased activity of glutamate decarboxylase).

Anorexia requires the patient's body weight to be below normal/underweight.

Hypochloremia, metabolic alkalosis, and hypokalemia (due to volume depletion).

Antipsychotic agents.

Acetylcholine. The basal nucleus of Meyneri is often affected.

Huntington's Chorea (or Huntington's Disease).

Symptoms that do not improve with an acetylcholinesterase inhibitor because the patient cannot synthesize acetylcholine.

Mood stabilizers (like lithium or lamotrigine), as they take too long to kick in.

Anorexia requires the patient's body weight to be below normal/underweight.

Hypochloremia, metabolic alkalosis, and hypokalemia (due to volume depletion).

Antipsychotic agents.

Acetylcholine. The basal nucleus of Meyneri is often affected.

Huntington's Chorea (or Huntington's Disease).

Symptoms that do not improve with an acetylcholinesterase inhibitor because the patient cannot synthesize acetylcholine.

Mood stabilizers (like lithium or lamotrigine), as they take too long to kick in.