Step 1 Complicated Concepts Thread

[TheSeanieB]

ASK AND ANSWER TOUGH QUESTIONS RELATED TO STEP 1.

Starting with me:
physiologic chloride shift - When CO2 diffuses into a RBC, it quickly converts with H2O to H+ and HCO3- so that CO2 will continue to passively diffuse into the RBC. The HCO3- is then excreted into the plasma by a Cl-/HCO3- exchanger. When the RBC enters the pulmonary capillaries, the process reverses. HCO3- is taken up by exchange for a Cl-. It combines with H+ to creates CO2 +H2O. The CO2 then diffuses out of the RBC and ultimately into the alveoli. This process allows for maximal CO2 excretion by a RBC.

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[Jamiu22]

Haha but I think the point is, he is thinking of the other woman while doing it

Maybe it would be sublimation if he went down on her lol

I was going to chime in.....but now all I can do is laugh

 

[JP2740]

Haha but I think the point is, he is thinking of the other woman while doing it

Maybe it would be sublimation if he went down on her lol

Lmfao

Are you even high yield bro?

 

[addo]

Haha but I think the point is, he is thinking of the other woman while doing it

Maybe it would be sublimation if he went down on her lol

that would be altruism as the satisfaction of going down on her would be enjoyed vicariously through introjection!

 

[WilliamsEph]

FA isn't clear on this. Different online sources have said either SSRI, TCA (Imipramine), or Benzo (Alprazolam).

Which does the step say is right?

 

[coolforschool]

FA isn't clear on this. Different online sources have said either SSRI, TCA (Imipramine), or Benzo (Alprazolam).

Which does the step say is right?

I've only ever heard of the SSRIs being the first line for pharmacologic treatment. The other one is CBT which is non-pharm, but I'm not sure which one is preferred.

 

[MLT2MT2DO]

FA isn't clear on this. Different online sources have said either SSRI, TCA (Imipramine), or Benzo (Alprazolam).

Which does the step say is right?

I've only ever heard of the SSRIs being the first line for pharmacologic treatment. The other one is CBT which is non-pharm, but I'm not sure which one is preferred.

Benzo's are used for acute anxiety, due to SSRIs takes 2-5 weeks to "kick in". TCA is now only used if SSRIs are ineffective due to the heinous side effects

 

[teratomas]

I know I have read somewhere than CN 2 is the only cranial nerve that is part of the CNS, but I just wanted to confirm..is CN 1 considered PNS? Or is it just the nerves that synapse onto the olfactory bulb?

 

[JP2740]

Had a uworld question. Read below in white

It said arsenic is specifically treated w/ dimercaprol and edta was incorrect. WHy is that? I was never taught that.

 

[coolforschool]

Benzo's are used for acute anxiety, due to SSRIs takes 2-5 weeks to "kick in". TCA is now only used if SSRIs are ineffective due to the heinous side effects

Good call, dude. Thanks.

@JP - We only learned that the latter treatment was for lead.

 

[loveoforganic2]

Had a uworld question. Read below in white

It said arsenic is specifically treated w/ dimercaprol and edta was incorrect. WHy is that? I was never taught that.

Explanations in that question also said that (white text follows) EDTA treats mercury poisoning, which I wasn't able to corroborate on searching. The dimercaprol thing for arsenic seemed to sync up with other sources though

 

[tiedyeddog]

Ok, got a question in UW that really pissed me off:

Basically, guy has massive diarrhea and vomiting over 24 hours, hasn't had any liquid intake. BP is 90/60, guy looks super hypovolemic.

How does GFR/ RPF/ FF change.

So I guessed they all decrease. turns out GFR RPF both decrease yet FF goes up. I understand the explanation but my question is in hypovolemia does it always occur like this?

 

[CrouchingLiger]

Ok, got a question in UW that really pissed me off:

Basically, guy has massive diarrhea and vomiting over 24 hours, hasn't had any liquid intake. BP is 90/60, guy looks super hypovolemic.

How does GFR/ RPF/ FF change.

So I guessed they all decrease. turns out GFR RPF both decrease yet FF goes up. I understand the explanation but my question is in hypovolemia does it always occur like this?

For the most part, yeah. The increased FF is from Angiotensin II, which constricts the efferent arteriole. That increases FF (if alone, that would increase GFR and have no change to RPF). The decreased perfusion pressure is causing a massive decrease in RPF and a proportional decrease in GFR, which is more significant than the ATII effect on GFR. However, the low perfusion pressure alone won't change FF until ATII comes along and causes it to increase.

 

[loveoforganic2]

Ok, got a question in UW that really pissed me off:

Basically, guy has massive diarrhea and vomiting over 24 hours, hasn't had any liquid intake. BP is 90/60, guy looks super hypovolemic.

How does GFR/ RPF/ FF change.

So I guessed they all decrease. turns out GFR RPF both decrease yet FF goes up. I understand the explanation but my question is in hypovolemia does it always occur like this?

Think about it this way - GFR = the desired effect. Variations in afferent and efferent arteriolar constriction are the means to achieving that effect. The desired effect is a constant 125 mL/min. Normally, we have more than enough perfusion (RPF), so we have a relatively low FF (GFR / RPF). This low FF at physiologic perfusion is a tolerance built into the body (just like everything, e.g. coronary arterioles normally not maximally dilated). At low perfusion, you react by using up some of that tolerance/intrinsic slack in the system

I'm sure you'd eventually reach a point where FF starts to decrease though (since 0 CO = 0 GFR), but I assume that happens pretty late in the game

 

[tiedyeddog]

For the most part, yeah. The increased FF is from Angiotensin II, which constricts the efferent arteriole. That increases FF (if alone, that would increase GFR and have no change to RPF). The decreased perfusion pressure is causing a massive decrease in RPF and a proportional decrease in GFR, which is more significant than the ATII effect on GFR. However, the low perfusion pressure alone won't change FF until ATII comes along and causes it to increase.

efferent arteriole constriction alone would increase GFR and decrease RPF, right? This scenario is then compound by afferent constriction from sympathetics driving both GFR and RPF down.

Think about it this way - GFR = the desired effect. Variations in afferent and efferent arteriolar constriction are the means to achieving that effect. The desired effect is a constant 125 mL/min. Normally, we have more than enough perfusion (RPF), so we have a relatively low FF (GFR / RPF). This low FF at physiologic perfusion is a tolerance built into the body (just like everything, e.g. coronary arterioles normally not maximally dilated). At low perfusion, you react by using up some of that tolerance/intrinsic slack in the system

I'm sure you'd eventually reach a point where FF starts to decrease though (since 0 CO = 0 GFR), but I assume that happens pretty late in the game

this makes sense, thanks for the explanation!!

 

[sharklasers]

How to distinguish between Kluver-Bucy syndrome (amygdala - hypororality, hypersecuality, disinhibited) from a prefrontal lobe lesion (can also cause similar symptoms, especially the disinhibited type).

Thanks!

 

[tiedyeddog]

I remember reading a good example differentiating projection from displacement. It's a good reminder that projection doesn't always have to appear "negative".

A married man sees an attractive woman when he's out with some friends and thinks about having sex with her. If he goes home to his wife (who was also out with her friends) and thinks that she may have cheated on him, that is projection. If instead he goes home and has sex with his wife, that is displacement

the more I read over the psych section of FA the more I think this subject of medicine is entirely made up bull****.

 

[Pinkleton]

How to distinguish between Kluver-Bucy syndrome (amygdala - hypororality, hypersecuality, disinhibited) from a prefrontal lobe lesion (can also cause similar symptoms, especially the disinhibited type).

Thanks!

The boards would make it obvious whether a patient has Kluver Bucy or a PFC lesion. If you see hyperorality, it has to be KB. Impaired cognition=PFC. As for hypersexuality, that is also KB. Although PFC lesion can make a pt disinhibited, I think they would present more as rude/blunt than sexually aggressive



Now I have an ethics Q. If a man has HIV and is having unprotected sex with his partner, your course of action is supposedly to encourage discussion before you tell her he has HIV. But what about the time period between you knowing and saying anything? How long is that? What if she contracts the disease in that time period? Seems like the man is basically attempting assault and you're being too understanding of it

 

[JP2740]

Just want to make sure, things like decreased CO, anemia, etc. can be classified as producing ischemia right? Or is ischemia purely based on blood flow, so wouldn't include anemia, CO poison etc

 

[JP2740]

One more, on pg.551, they're talking v/q mismatches, and then they refer to airway obstruction as a shunt. What the hell do they mean? Why would that make a v/q -> 0

 

[loveoforganic2]

Just want to make sure, things like decreased CO, anemia, etc. can be classified as producing ischemia right? Or is ischemia purely based on blood flow, so wouldn't include anemia, CO poison etc

Hypoxia - Low O2 delivery; includes below 3
Ischemia - Low blood flow
Hypoxemia - Low partial pressure of O2
Decreased O2 carrying capacity (your examples would be in this category)

 

[Pinkleton]

One more, on pg.551, they're talking v/q mismatches, and then they refer to airway obstruction as a shunt. What the hell do they mean? Why would that make a v/q -> 0

Let's say you obstruct a lobe of the lung. Your V drops big time because air cannot get in. So your v/q plummets. You quickly have hypoxic vasoconstriction which reduces the Q, but not completely so you still have a lowered v/q. A lower v/q implies a R to L shunt because your PaO2 is lower...since that area receiving no oxygen is still slightly perfused

 

[Jamiu22]

Let's say you obstruct a lobe of the lung. Your V drops big time because air cannot get in. So your v/q plummets. You quickly have hypoxic vasoconstriction which reduces the Q, but not completely so you still have a lowered v/q. A lower v/q implies a R to L shunt because your PaO2 is lower

Thanks man... I've always wondered about that - and never got it.

 

[CrouchingLiger]

One more, on pg.551, they're talking v/q mismatches, and then they refer to airway obstruction as a shunt. What the hell do they mean? Why would that make a v/q -> 0

V = ventilation, so if there is an obstruction in the airway, the alveoli distal to the obstruction are getting zero ventilation. v/q = 0/q= 0. This is, by definition, a shunt, based on the calculation of v/q. Also, you can think of a shunt this way: any blood that reaches the left atrium without getting oxygenated gets there by being "shunted" without being re-oxygenated. The blood that passes by those alveoli that are blocked will not get any oxygen (because no fresh air is getting to those alveoli). Blood is still running through those capillaries, and they return to the left atrium without any more oxygen. This is why a shunt causes decreased PaO2, because there is unoxygenated blood mixing with the properly oxygenated blood before it reaches the arteries.

Not sure if I helped this make sense or just made it more confusing. Contrast this with, for example, a PE that causes an increased alveolar dead space (v/q = undefined), but doesn't decease oxygen levels of any of the blood reaching the left side of the heart, so its not a shunt.

 

[Pinkleton]

I'm having a hard time accepting that nitrates increase contractility via reflex. So they increase contractility and heart rate, but reduce preload. This must mean that SV still drops? I figured that contractility and heart rate would outweigh a fall in preload...

edit: ALSO, can someone explain the effect of Vit D on bone? FA says its causes bone breakdown (I assume this is old bone)? Does it do this indirectly through osteoblasts (like PTH) or directly on osteoclasts

What about promoting bone mineralization? I always thought Vit D promotes mineralization of new bone but that is not mentioned in FA

 

[JP2740]

V = ventilation, so if there is an obstruction in the airway, the alveoli distal to the obstruction are getting zero ventilation. v/q = 0/q= 0. This is, by definition, a shunt, based on the calculation of v/q. Also, you can think of a shunt this way: any blood that reaches the left atrium without getting oxygenated gets there by being "shunted" without being re-oxygenated. The blood that passes by those alveoli that are blocked will not get any oxygen (because no fresh air is getting to those alveoli). Blood is still running through those capillaries, and they return to the left atrium without any more oxygen. This is why a shunt causes decreased PaO2, because there is unoxygenated blood mixing with the properly oxygenated blood before it reaches the arteries.

Not sure if I helped this make sense or just made it more confusing. Contrast this with, for example, a PE that causes an increased alveolar dead space (v/q = undefined), but doesn't decease oxygen levels of any of the blood reaching the left side of the heart, so its not a shunt.

Ok cool. So basically the R->L shunt is not the same R->L of a heart but the same idea because the blood in either case is not getting oxygenated as much in either case, right?

About v/q -> infinity. The oxygen levels will be fine? That last paragraph kind of threw me.

 

[JP2740]

edit: ALSO, can someone explain the effect of Vit D on bone? FA says its causes bone breakdown (I assume this is old bone)? Does it do this indirectly through osteoblasts (like PTH) or directly on osteoclasts

What about promoting bone mineralization? I always thought Vit D promotes mineralization of new bone but that is not mentioned in FA

Technically, vit D promotes bone resorption directly, but since it increases Ca and P in the blood, it's overall effect is to promote bone formation albeit indirectly.

One of my teachers (who's actually brilliant) described it as with low Ca/P levels -> promotes bone resorption (gets the levels up), but with normal Ca/P -> necessary to mineralize osteoid as the functions of vit-d

 

[JP2740]

pg. 554 classic triad hypoxemia, neuro abnormality, pretechial rash- is this the classic triad of a fat emboli or a pulmonary embolism lol

 

[Pinkleton]

pg. 554 classic triad hypoxemia, neuro abnormality, pretechial rash- is this the classic triad of a fat emboli or a pulmonary embolism lol

I believe it is fat emoblism. Can't think of a reason why you would have petechial rash with other emboli. I would guess that tiny fat particles clog up all sorts of microvessels, including the skin and maybe cause these vessels to burst and produce pinpoint bleeds. Probably the same concept with neuro abnormalities, which I assume means stroke like symptoms rather than general neuro signs like confusion from hypoxia or something


Another question (still would like an answer for my nitrate question above lol):

Ok so I understand that highly protein bound drugs like hydralazine increase the risk for drug-induced lupus because they're floating around in the blood. This would mean they are lipophilic correct?

So what about another hydrophilic drug like THC that distributes widely into tissues because it is lipophilic. Does that mean it is also highly plasma protein bound?

I guess it seems contradictory to me that a lipophilic drug both distributes widely throughout body tissues yet is also highly protein bound

 

[JP2740]

What's the difference between a case-control study and a RETROspective cohort study?

 

[Jamiu22]

What's the difference between a case-control study and a RETROspective cohort study?

With the little I know about this stuff... to me they seem the same but the questions I've seen usually tell you what they are trying to assess... whether it be relative risk or odds ratio (retrospective cohort for the former and case control for the latter)...

... someone else can probably chime in with more specifics.. I'd like to know

 

[coolforschool]

I'm having a hard time accepting that nitrates increase contractility via reflex. So they increase contractility and heart rate, but reduce preload. This must mean that SV still drops? I figured that contractility and heart rate would outweigh a fall in preload...

Not sure what you're asking, tbh. Nitrates vasodilate --> decrease preload --> reduced LVEDV/myocardial stretch --> less MVO2 (decreased work) --> patients feel better. I think what you're asking is that shouldn't the reflex contractility and tachycardia increase the SV and thus cancel the fall in preload, and I'm not sure. I would think that less blood coming into the heart due to venous pooling would negate any increases in the HR/contractility/SV since there's a lower amount of blood --> less myocardial stretch and hence less MVO2 consumption. Not sure.

Ok so I understand that highly protein bound drugs like hydralazine increase the risk for drug-induced lupus because they're floating around in the blood. This would mean they are lipophilic correct?

So what about another hydrophilic drug like THC that distributes widely into tissues because it is lipophilic. Does that mean it is also highly plasma protein bound?

I guess it seems contradictory to me that a lipophilic drug both distributes widely throughout body tissues yet is also highly protein bound

Yeah, THC is definitely highly protein-bound, but I'm not sure how that affects its distribution. Protein-bound drugs can't exert their effects, but at the same time they can't be metabolized. So maybe eventually they distribute? Idk.

What's the difference between a case-control study and a RETROspective cohort study?

With the little I know about this stuff... to me they seem the same but the questions I've seen usually tell you what they are trying to assess... whether it be relative risk or odds ratio (retrospective cohort for the latter and case control for the former)...

... someone else can probably chime in with more specifics.. I'd like to know

Case-control is odds ratio --> the ODDS that the exposure caused the disease. So you're starting with the disease in patients, but looking for an exposure that may have caused the disease, hence the ODDS that that exposure caused the disease.

Cohort study is relative risk --> the RISK of developing a disease if you have been exposed. So you're starting with the exposure in patients and looking for the risk of developing disease; you're looking for the RISK of getting a disease from an exposure.

Retrospective cohort: it's still the same concept, except that you're looking through medical records. So you're looking at patients who were exposed vs. non-exposed and looking to see who developed the disease.

Let me know if I'm wrong. I'm close to my test date.

 

[Jamiu22]

Not sure what you're asking, tbh. Nitrates vasodilate --> decrease preload --> reduced LVEDV/myocardial stretch --> less MVO2 (decreased work) --> patients feel better. I think what you're asking is that shouldn't the reflex contractility and tachycardia increase the SV and thus cancel the fall in preload, and I'm not sure. I would think that less blood coming into the heart due to venous pooling would negate any increases in the HR/contractility/SV since there's a lower amount of blood --> less myocardial stretch and hence less MVO2 consumption. Not sure.



Yeah, THC is definitely highly protein-bound, but I'm not sure how that affects its distribution. Protein-bound drugs can't exert their effects, but at the same time they can't be metabolized. So maybe eventually they distribute? Idk.





Case-control is odds ratio --> the ODDS that the exposure caused the disease. So you're starting with the disease in patients, but looking for an exposure that may have caused the disease, hence the ODDS that that exposure caused the disease.

Cohort study is relative risk --> the RISK of developing a disease if you have been exposed. So you're starting with the exposure in patients and looking for the risk of developing disease; you're looking for the RISK of getting a disease from an exposure.

Retrospective cohort: it's still the same concept, except that you're looking through medical records. So you're looking at patients who were exposed vs. non-exposed and looking to see who developed the disease.

Let me know if I'm wrong. I'm close to my test date.

Nope... you got it exactly, and eloquent (my hands sometimes type faster,... than my brain)...

 

[JP2740]

Ok here's two more you intelligent bastards. Crossover study - each patient acts as their own control. What in the hell?

And in first aid pg.55 confidence intervals, they're using mean - Z (SEM). And then they say for 95% CI, Z = 1.96 for example. What in the world is Z, and is it's absolute value important? And I know what SEM is calculation wise, but can anyone conceptualize it for me?

 

[sharklasers]

Ok here's two more you intelligent bastards. Crossover study - each patient acts as their own control. What in the hell?

Patient is given the actual drug. Effect is noted.

Some period elapses to allow the patient to go back to baseline.

Same patient is given a placebo. Effect is noted.

These two effects are compared.

So instead of giving a select group of patients a placebo and a select group of patients the actual drug, you just give the same patient both, at different times. I think this is done to minimize confounding bias?

 

[sharklasers]

And in first aid pg.55 confidence intervals, they're using mean - Z (SEM). And then they say for 95% CI, Z = 1.96 for example. What in the world is Z, and is it's absolute value important? And I know what SEM is calculation wise, but can anyone conceptualize it for me?

And I really can't help you here. I am sure the answer will be well beyond what we would be required to know, if that is any help.

The way I think about it, the Z-score is just an arbitrary number (I know its really not) that is required to calculate confidence interval haha.

This might help though. If the Z score is higher (~2.5 or whatever instead of ~2), that would increase the confidence interval. Using the Z score of 2.5 would let you give you a confidence interval and let you say that there is a 99% chance the actual value falls within that interval.

With a smaller Z score, the confidence interval is smaller, and you are less sure that the actual value falls within that range. With a Z score of 2, you can only be 95% sure the value falls within that range.

 

[Jonari]

And I really can't help you here. I am sure the answer will be well beyond what we would be required to know, if that is any help.

The way I think about it, the Z-score is just an arbitrary number (I know its really not) that is required to calculate confidence interval haha.

This might help though. If the Z score is higher (~2.5 or whatever instead of ~2), that would increase the confidence interval. Using the Z score of 2.5 would let you give you a confidence interval and let you say that there is a 99% chance the actual value falls within that interval.

With a smaller Z score, the confidence interval is smaller, and you are less sure that the actual value falls within that range. With a Z score of 2, you can only be 95% sure the value falls within that range.

this really is the best explanation for Z...they'll give it to you in the stem saying 95% CI or 99% CI, which equals to a Z value of 2 or 2.5, respectively.

can anybody clarify if it's 2 and 2.5, respectively...just had a brain fart

 

[sharklasers]

this really is the best explanation for Z...they'll give it to you in the stem saying 95% CI or 99% CI, which equals to a Z value of 2 or 2.5, respectively.

can anybody clarify if it's 2 and 2.5, respectively...just had a brain fart

1.96 and 2.58, but i'm sure any calculation we would have to do, we can estimate!

 

[Jamiu22]

this really is the best explanation for Z...they'll give it to you in the stem saying 95% CI or 99% CI, which equals to a Z value of 2 or 2.5, respectively.

can anybody clarify if it's 2 and 2.5, respectively...just had a brain fart

1.96 and 2.58 to be exact.....but its easier to remember the numbers sharklaser's saying... I really think this is beyond step1.. but I would have to say I saw a couple of questions on kaplan about this very thing..

They essentially gave a mean, standard deviation (stdev) varying experiments (number = n)..and they wanted to find out 95% that CI of our data....

So first, you calc. SEM.... then from there, just straight up use the equation in FA.. it was quite easy actually.

 

[Jonari]

1.96 and 2.58, but i'm sure any calculation we would have to do, we can estimate!

1.96 and 2.58 to be exact.....but its easier to remember the numbers sharklaser's saying... I really think this is beyond step1.. but I would have to say I saw a couple of questions on kaplan about this very thing..

They essentially gave a mean, standard deviation (stdev) varying experiments (number = n)..and they wanted to find out 95% that CI of our data....

So first, you calc. SEM.... then from there, just straight up use the equation in FA.. it was quite easy actually.

no and yes to both what you guys are saying...it's 1.96 and 2.58, but Kaplan biostats says not to use those figures and use 2 and 2.5 instead as substitues, respectively.

 

[Jonari]

 

[sharklasers]

no and yes to both what you guys are saying...it's 1.96 and 2.58, but Kaplan biostats says not to use those figures and use 2 and 2.5 instead as substitues, respectively.

just wondering, how is that "no" to what either of us is saying? lol

not that it really matters, just curious

just because both of us said it would be easier to use 2 and 2.5, like kaplan says

 

[Jonari]

just wondering, how is that "no" to what either of us is saying? lol

not that it really matters, just curious

just because both of us said it would be easier to use 2 and 2.5, like kaplan says

beat me to it..yeah i was in the process of editing it out, after i uploaded the pic...i forgot that 2 and 2.5 are the rounded figures, not the exact figures which the 95% and 99% CI indicate

 

[coolforschool]

just wondering, how is that "no" to what either of us is saying? lol

not that it really matters, just curious

just because both of us said it would be easier to use 2 and 2.5, like kaplan says

beat me to it..yeah i was in the process of editing it out, after i uploaded the pic...i forgot that 2 and 2.5 are the rounded figures, not the exact figures which the 95% and 99% CI indicate

I haven't been through the biostats chapter yet. Can you guys explain all of that using an example? I understand all of the terms individually (e.g., what CI means), but I haven't run into many questions that would test your knowledge, like how to manipulate or calculate one value using the others.

 

[dbeast]

Hope this one hasn't been asked yet, but does anybody have a good way to keep the seizure meds straight? Seriously... 3 different "1st line" drugs for tonic-clonic?

 

[TheSeanieB]

Do anyone have any ideas as to why aminoglycoside have much better activity on the gram- rods that on gram - cocci? Essentially why does the shape of the bacteria change the efficacy of the medication?

 

[sharklasers]

Hope this one hasn't been asked yet, but does anybody have a good way to keep the seizure meds straight? Seriously... 3 different "1st line" drugs for tonic-clonic?

hmm i'm assuming they would have more than just tonic clonic though.

if there is any clue of it the patient being status epilepticus, give phenytoin. for tonic clonic with any other seizure types, or maybe even trigeminal neuralgia give carbamazepine, for tonic clonic with absence or myoclonic seizures, give valproic.

im sure that doesn't help since its all written in first aid, but basically, i tried to focus on where their differences lie, not so much that giant chart of check marks.

for example, i don't really know anything about what kind of seizures topiramate are used for, but I do know it is used for migraine prevention.

and same with phenobarbital, but that its used in children etc

 

[MLT2MT2DO]

Do anyone have any ideas as to why aminoglycoside have much better activity on the gram- rods that on gram - cocci? Essentially why does the shape of the bacteria change the efficacy of the medication?

My assumption has always been the thinner cell wall of GN. The reason penicillins/amino's work so well synergistically is the penicillin will weaken the GP cell wall and allow Aminoglycosides to diffuse more readily. Gram Negatives start with a thinner wall so less to diffuse through.

The synergistic comment I know I have correct. The Gram Negative comments were assumptions, putting pieces together.

 

[Jonari]

hmm i'm assuming they would have more than just tonic clonic though.

if there is any clue of it the patient being status epilepticus, give phenytoin. for tonic clonic with any other seizure types, or maybe even trigeminal neuralgia give carbamazepine, for tonic clonic with absence or myoclonic seizures, give valproic.

im sure that doesn't help since its all written in first aid, but basically, i tried to focus on where their differences lie, not so much that giant chart of check marks.

for example, i don't really know anything about what kind of seizures topiramate are used for, but I do know it is used for migraine prevention.

and same with phenobarbital, but that its used in children etc

i can't even get the type of seizures that they're describing in the question, to solve for which medication to use, unless it gives the hint that the seizures is over 30 minutes...then i know it's status epilepticus...but otherwise...i'm 0/several of these

any good input on how to differentiate these seizures when given in them stem of a question...? thanks!

 

[sharklasers]

i can't even get the type of seizures that they're describing in the question, to solve for which medication to use, unless it gives the hint that the seizures is over 30 minutes...then i know it's status epilepticus...but otherwise...i'm 0/several of these

any good input on how to differentiate these seizures when given in them stem of a question...? thanks!

Hmm it's been a while since I've seen seizure questions I don't have much help. Ill remember to keep this in mind for later.

But,

Blank stare = absence - this is probably the most important
You got status epileptics.
Myoclonic - think tic-like use valproate
Tonic - stiffening
Tonic-clonic = above two combined

I guess this is kind of what first aid gives you but again, Ill look out for these questions so I can get a refresher on how I personally approach seizures given certain information.

 

[Jonari]

Hmm it's been a while since I've seen seizure questions I don't have much help. Ill remember to keep this in mind for later.

But,

Blank stare = absence - this is probably the most important
You got status epileptics.
Myoclonic - think tic-like use valproate
Tonic - stiffening
Tonic-clonic = above two combined

I guess this is kind of what first aid gives you but again, Ill look out for these questions so I can get a refresher on how I personally approach seizures given certain information.

thanks bud!

another question for discussion...it's a NBME spoiler question so highlight the text below to see it...easy concept, but why am i being a potato about it?
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last warning - **NBME 6 SPOILERS** - highlight text to see the question

patient is basically taking benzos for anxiety. his history shows he has a duodenal ulcer. obviously mcc of duodenal ulcers is h. pylori. patient tells you the drug is working really well and he's falling asleep very fast. which other drug is causing this.

basically a cyp450 inhibitor

i wrote omeprazole...wrong lol, answer is cimetidine...

kaplan says omeprazole is a cyp450 inhibitor but it's not in FA...was the drug recently removed from the list