Neuro/Psych Pharm

[mdeast]

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Doing some UWorld Neuro/Psych questions and about 75% seem to be killer pharm related questions. My medical school did an absolutely terrible job teaching us neuro/psych drugs (we basically did 90% pathology in our neuro block) and I'm pretty clueless on most of these...particularly all the obscure (at least to me?) side effects and drug interactions that they seem to be testing.

How much time should I spend trying to correct my lack of knowledge? (i.e. how high yield will it be to devote a lot of time to learning these drugs?).

 

[shan564]

I think you can probably learn those drugs in less time than you think. There are long lists of drugs, but for the most part, you can organize them into classes. For instance, carbamazepine/phenytoin/valproate have somewhat different MOAs, but they're all first-line drugs for epilepsy and they all cause birth defects.

There's also a list of drug interactions in FA. You should probably know all of those. There are a lot of neuro/psych drugs in there.

I think it's fairly high-yield to have a solid knowledge of the 3-5 pages of pharm in First Aid's neuro and psych sections. I doubt that you'll need more than that. I think the only low-yield thing in those sections is the anesthetics, but they're still fair game too.

I generally like to divide up the drugs by the neurotransmitter that they effect. That helps keep the side effects straight. For instance:

GABA: receptor activated by benzos, barbiturates, zolpidem (Ambien), ethanol
Serotonin: increased by SSRIs, SNRIs/TCAs, MAOIs; blocked by mirtazapine
Dopamine: increased by L-dopa, buproprion, MAOIs; decreased by antipsychotics/neuroleptics
Opioid: potentiated by drugs with "morph" or "cod" in their names, partially agonized by buprenorphine, blocked by naloxone/naltrexone
NE: increased by amphetamines, cocaine, MAOIs, mirtazapine
ACh: increased by AChEIs (for Alzheimer's), blocked by anticholinergics (for Parkinson's) and neuromuscular blockers

And that covers pretty much everything except for the seizure drugs (haven't found a shortcut for these), the anesthetics (probably not too high-yield beyond basic principles and simple mnemonics), and the glaucoma drugs (know them cold, but it's a pretty short list and you should already be familiar with most of those drugs from their other uses).

 

[mdeast]

Grrr. I think it's just my overall dislike of pharmacology (just seems like a lot of useless rote memorization, but seemingly easy points on Boards if you can get it down).

Thanks for the help though 🙂 Why are the glaucoma drugs so important again? So far my overall drug learning goals have been (1) Antibiotics (2) Autonomic (3) Cardio-Vascular/Renal/Pulmonary (4) everything else....

 

[shan564]

Glaucoma drugs are just one of those things that happen to be particularly high-yield. I think it's because it requires you to integrate a lot of concepts/systems, since pretty much all five of the glaucoma drug classes were originally intended for other purposes, which means that they have a lot of interactions and contraindications. And glaucoma is a very common condition.

I think I can summarize most of what you need to know about glaucoma drugs. There are five classes:

1. Alpha agonists (i.e. epinephrine) - contraindicated in acute angle closure glaucoma because they cause mydriasis, which puts more pressure on the blockage. Also contraindicated in hypertension for obvious reasons.

2. Beta blockers (i.e. timolol) - contraindicated whenever beta blockers are contraindicated for other reasons.

3. Diuretics (i.e. acetazolamide, mannitol) - DOC in angle closure, but contraindicated wherever acetazolamide/mannitol are contraindicated.

4. Prostaglandin analogs (i.e. latanoprost) - usually the DOC in outpatient management of open-angle glaucoma.

5. Cholinergics (i.e. pilocarpine) - contraindicated wherever cholinergics are contraindicated.


Also, if you find pharmacology to be largely about rote memorization, then you might be approaching it the wrong way. I mean, yes, you have to memorize the names of the drugs, but a large portion of them have a suffix or root that give away their function. The side effect profiles and indications/contraindications can usually be inferred from the MOA.

But that's just my opinion. I feel like everything in medicine requires excessive rote memorization except for physio, path, and pharm. Micro, biochem, anatomy, and embryo all just seem like long lists of stuff that won't be particularly useful in the real world... yes, I need to know that Corynebacterium diphtheriae causes psuedomembranous pharyngitis, but when will I ever use the knowledge that its toxin works via ADP ribosylation through EF-2? On the other hand, if I'm a GP who has a patient with a random drug reaction/interaction, I should be able to recognize it. Or if I need to write a prescription for somebody with lots of comorbidities (like the frequent-flyer patients who make up most of our clinical practice), I should know which drugs to avoid.

 

[mdeast]

Glaucoma drugs are just one of those things that happen to be particularly high-yield. I think it's because it requires you to integrate a lot of concepts/systems, since pretty much all five of the glaucoma drug classes were originally intended for other purposes, which means that they have a lot of interactions and contraindications. And glaucoma is a very common condition.

I think I can summarize most of what you need to know about glaucoma drugs. There are five classes:

1. Alpha agonists (i.e. epinephrine) - contraindicated in acute angle closure glaucoma because they cause mydriasis, which puts more pressure on the blockage. Also contraindicated in hypertension for obvious reasons.

2. Beta blockers (i.e. timolol) - contraindicated whenever beta blockers are contraindicated for other reasons.

3. Diuretics (i.e. acetazolamide, mannitol) - DOC in angle closure, but contraindicated wherever acetazolamide/mannitol are contraindicated.

4. Prostaglandin analogs (i.e. latanoprost) - usually the DOC in outpatient management of open-angle glaucoma.

5. Cholinergics (i.e. pilocarpine) - contraindicated wherever cholinergics are contraindicated.


Also, if you find pharmacology to be largely about rote memorization, then you might be approaching it the wrong way. I mean, yes, you have to memorize the names of the drugs, but a large portion of them have a suffix or root that give away their function. The side effect profiles and indications/contraindications can usually be inferred from the MOA.

But that's just my opinion. I feel like everything in medicine requires excessive rote memorization except for physio, path, and pharm. Micro, biochem, anatomy, and embryo all just seem like long lists of stuff that won't be particularly useful in the real world... yes, I need to know that Corynebacterium diphtheriae causes psuedomembranous pharyngitis, but when will I ever use the knowledge that its toxin works via ADP ribosylation through EF-2? On the other hand, if I'm a GP who has a patient with a random drug reaction/interaction, I should be able to recognize it. Or if I need to write a prescription for somebody with lots of comorbidities (like the frequent-flyer patients who make up most of our clinical practice), I should know which drugs to avoid.

Well, I definitely agree some side effects can be inferred by the mechanism of the drug. I'm usually OK reasoning those out. But, for instance....Phenytoin causes Gingival Hyperplasia and SLE syndrome. I don't see a clear connections given the MOA alone. Or, lamotrigine causes Steven Johnson syndrome. Again, not clear in the MOA. Just seems like rote memorization to me and I never feel these are questions that really test your knowledge of how the body (and/or treatments) work.

I think it's also exacerbated by the pharm curriculum at my institution. We don't have a formal pharmacology class as part of our pre-clinical years. It's integrated into the organ system. We also spent very little time on it and weren't really asked to memorize much besides MOA of prototypical drugs in each class (i.e. there are 10 different benzo's with different uses, but we never learned anything more than diazepam and lorazepam....and even then, side effects would rarely be a question on our exam unless they were extremely common- i.e. ACE Inhibitors= cough, SSRIs= sexual dysfunction).

Anyway, thanks for the help! Venting never gets you anywhere. Gotta learn these drugs 😉

 

[shan564]

Well, I definitely agree some side effects can be inferred by the mechanism of the drug. I'm usually OK reasoning those out. But, for instance....Phenytoin causes Gingival Hyperplasia and SLE syndrome. I don't see a clear connections given the MOA alone. Or, lamotrigine causes Steven Johnson syndrome. Again, not clear in the MOA. Just seems like rote memorization to me and I never feel these are questions that really test your knowledge of how the body (and/or treatments) work.

Yeah, there's definitely some memorization there, but I feel like it's a lot less memorization than subjects like micro/anatomy/embryo. But I guess it's just different ways of looking at things.

I think it's also exacerbated by the pharm curriculum at my institution. We don't have a formal pharmacology class as part of our pre-clinical years. It's integrated into the organ system. We also spent very little time on it and weren't really asked to memorize much besides MOA of prototypical drugs in each class (i.e. there are 10 different benzo's with different uses, but we never learned anything more than diazepam and lorazepam....and even then, side effects would rarely be a question on our exam unless they were extremely common- i.e. ACE Inhibitors= cough, SSRIs= sexual dysfunction).

Yeah, our curriculum was the same because my school is in Australia, so they don't care if their students pass the USMLE. We knew about the deficiencies, so I got together with some other North American students and we learned pharm independently during 2nd year with the help of Kaplan and First Aid. If you have time, I think the Kaplan pharm videos with Lionel Raymon (I watched the 2007 edition) are an excellent way to make up for a deficient pharm curriculum.

Anyway, thanks for the help! Venting never gets you anywhere. Gotta learn these drugs 😉

Venting can be therapeutic... 😀

 

[hoodfigga1]

omg i $*%^&$* hate going thru seizure drugs....any1 have a way to keep them straight? not so much with MOA but wen to use wat (i.e. DOC in absent, complex, simple, etc.)....

just looking at that FA page hurts...........much appreciated

 

[shan564]

I don't like the way that seizure DOC's are organized in FA. There are really only a few things to know.

Absence seizures - DOC is ethosuximide

Status epilepticus - DOC is benzos for the acute condition and phenytoin for prophylaxis

Partial seizures (simple or complex) - DOC is carbamaezepine

Tonic-clonic seizures - DOC is carbamazepine, phenytoin, or valproate




To put it another way...
Benzos - DOC for acute status epilepticus (or eclampsia)
Ethosuximide - DOC for absence seizures
Carbamazepine - DOC for tonic-clonic and partial seizures, and also possibly trigeminal neuralgia
Valproate and Phenytoin - DOC for tonic-clonic seizures

Everything else is used as second/third/fourth-line drugs.

 

[hoodfigga1]

I don't like the way that seizure DOC's are organized in FA. There are really only a few things to know.

Absence seizures - DOC is ethosuximide

Status epilepticus - DOC is benzos for the acute condition and phenytoin for prophylaxis

Partial seizures (simple or complex) - DOC is carbamaezepine

Tonic-clonic seizures - DOC is carbamazepine, phenytoin, or valproate




To put it another way...
Benzos - DOC for acute status epilepticus (or eclampsia)
Ethosuximide - DOC for absence seizures
Carbamazepine - DOC for tonic-clonic and partial seizures, and also possibly trigeminal neuralgia
Valproate and Phenytoin - DOC for tonic-clonic seizures

Everything else is used as second/third/fourth-line drugs.

thanks a lot man. i realized the simplicity comes once u dont look at that chart lol

quick follow up question.. i remember a uworld question where a patient had both tonic-clonic + absence seizures which made the tx answer valproate because it can be used in both whereas carbamazepine shoudnt be used in absent

with that being said have u encountered or is it possible for questions to have a patient with JUST tonic-clonic?? in other words, how would u choose a DOC when more than 1 drug is considered 1st line??

 

[JasonE]

ya theres an easy way to do it.

just know phenytoin, carbemazepine, valproic acid

and then ethosuxamide for absence seizures


the rest of the drugs are low yield (straight from lionel) and much less likely to show up on your exam. not worth the headache. i also dont think you really need to know what drugs to use for what type of seizure. i know it showed up on UWORLD, but i just dont see that coming up on the real exam. please correct me if im wrong

thats the problem with first aid. sometimes its hard to tell whats more important than other things when its all in a table

 

[mdeast]

thanks a lot man. i realized the simplicity comes once u dont look at that chart lol

quick follow up question.. i remember a uworld question where a patient had both tonic-clonic + absence seizures which made the tx answer valproate because it can be used in both whereas carbamazepine shoudnt be used in absent

with that being said have u encountered or is it possible for questions to have a patient with JUST tonic-clonic?? in other words, how would u choose a DOC when more than 1 drug is considered 1st line??

I remember that question as well and thought it was really meant to make your "learn" the drugs rather than representative of a boards type question. In general, valproate is known as the "general" seizure medication....meaning it can effectively treat most seizures even though it might not be the first line therapy for single phenotype seizures.

 

[hoodfigga1]

appreciate the help guys. ya i am sticking to the minimalist approach in terms of learning them for now, just hoping they wont get any more specific..

mayb its no coincidence goljan doesnt have much about seizures in RR...

 

[alternatego]

awesome thread

 

[Phloston]

Status epilepticus - DOC is benzos for the acute condition and phenytoin for prophylaxis.

Status epilepticus - DOC is benzos for the acute condition and phenytoin for prophylaxis AND seizures refractory to benzos; fosphenytoin versus phenytoin is preferred via IV due to increased H2O-solubility.

 

[faisal 2000]

tx of Parkinson:
Levodopa should not be given to psychotic patients because it may exacerbate the mental disturbance. It is also contraindicated in patients with
angle-closure glaucoma, but it is fine to use it with chronic open-angle glaucoma if intraocular pressure is well controlled and can be monitored. It is best given combined with carbidopa to patients with cardiac disease; even so, the risk of cardiac dysrhythmia is slight.
Vitamin B6 supplementa should not be taken by those on levodopa therapy , because B6 increases the peripheral metabolism of levodopa and decreases its effectiveness .

tx of Tourette’s syndrome: Haloperidol (1st line) which blocks D2 receptor and it has atropine like action, so the side effects of it are
parkinson, gynecomastia , galactorrhea, aminorrhea, dryness of the mouth, blurred vision, and gastrointestinal disturbances, tradive dyskinesia ( late in treatment) , neuroleptic malignant syndrome ( high fever, sweating, increase pulse and blood pressure, dystonea). neuroleptic malignant syndrome occurs early in treatment.

 

[faisal 2000]

neuroleptic malignant syndrome mainly caused by Halopridole, molindone and Metoclopramide. clinical findings are high fever, sweating, increase pulse and blood pressure, dystonea, elevated creatine kinase,rhabdomyolysis, sustained muscle contraction and rigidity. mechanism which responsible for that is disruption of intracelluar calcium metabolism due to hyperactivity of ryanodine receptor(calcium release channel) or dihydropyridine receptor.
treated by dantrolene or Dopamine agonists (eg, bromocriptine,cabergoline).
by the way Dopamine agonists (eg, bromocriptine, cabergoline) used for treatment of hyperprolactinemia.

malignant hyperthermia ; predisposed by Halothane and succinylcholine. characterized by sustained muscle contraction and rigidity, fever, acidosis, muscle necrosis, rhabdomyolysis and may produce myoglobinurea, tachycardia, hyperkalemia and hypercalcemia that accompany muscle necrosis. mechanism which responsible for that is (same as neuroleptic malignant syndrome) disruption of intracelluar calcium metabolism due to hyperactivity of ryanodine receptor(calcium release channel) or dihydropyridine receptor. treated by (IV) dantrolene which blocks ryanodine channel.

 

[faisal 2000]

tx of insomnia ;

1) behavior therapy (1st choice) such as daily exercise, avoid caffeine, and relaxation technique ...etc.
2) pharmacological treatment : using drugs that act on GAPA receptors or melatonin receptors.
drugs acting on GAPA : zolpidem (Ambien), zalplone(Sonata), eszopilone(Lunesta). they have short half-lives.
side effects of these drugs: hang over, impaired thinking, and insomnia rebound.
drug acting on melatonin receptor: ramelton will increase sleep desire. it does not have hang over, impaired thinking, insomnia rebound.

 

[DrPicard]

Is carbamazepine one of the DoCs for tonic clonic? I was under the impression only phenytoin and valproate were (at least thats how I remember FA puts it).

Also to the thread starter, neuro/psych pharma may seem daunting when you go through it first (all alien names + everything acting on the same few receptors), but if you can organize the information well, the second time through should be much, much easier. Trying to memorize as you come across these drugs in UWorld is going to be significantly more difficult since you lack that background classification to pin it on.

Kind of like how those micro cards classification tables make memorizing stuff so much easier.