Mycobacterium leprae = Leprosy

[MudPhud20XX]

Hi all, so I'm finally starting to preview micro, path, and pharm before my 2nd year starts this fall. Hopefully this effort will make my 2nd year less painful.

I would really appreciate it if you guys can help me out with some of questions that seem to be stupid and simple. (as always, I'm thankful for those who help me out!)

Alright so, Kaplan micro says:

1. M. tuberculosis with normal CD4 count or with low CD4 count (disseminated)
2. MAI only late with low CD4 count

My questions are:
1. So the reason you may expect low CD4 T cell count is b/c M. tuberculosis is an intracellular pathogen that triggers CD8 cytotoxic T cells and TH1 helper that makes IFN which stimulates macrophage, right?
2. What do you meant by "disseminated?" How does this make low CD4 count?
3. What does MAI stand for? And why does that give low CD4 count?
4. I've always thought that CD8 cytotoxic cells kill virus infected cells. But do they also killed some of the intracellular pathogen infected cells by any chance? If not, why not?

Many thanks in advance.

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[ulikedaggers]

Hi all, so I'm finally starting to preview micro, path, and pharm before my 2nd year starts this fall. Hopefully this effort will make my 2nd year less painful.

I would really appreciate it if you guys can help me out with some of questions that seem to be stupid and simple. (as always, I'm thankful for those who help me out!)

Alright so, Kaplan micro says:

1. M. tuberculosis with normal CD4 count or with low CD4 count (disseminated)
2. MAI only late with low CD4 count

My questions are:
1. So the reason you may expect low CD4 T cell count is b/c M. tuberculosis is an intracellular pathogen that triggers CD8 cytotoxic T cells and TH1 helper that makes IFN which stimulates macrophage, right?
2. What do you meant by "disseminated?" How does this make low CD4 count?
3. What does MAI stand for? And why does that give low CD4 count?
4. I've always thought that CD8 cytotoxic cells kill virus infected cells. But do they also killed some of the intracellular pathogen infected cells by any chance? If not, why not?

Many thanks in advance.

I had no idea you were an M1 too.

MAI is mycobacterium avium-intracellulare. I believe Kaplan is saying that MAI is only present when CD4 is low because MAI is an opportunistic organism. I don't know about the other stuff though.
http://emedicine.medscape.com/article/222664-overview

 

[Transposony]

Think it other way around.
Normal CD4 count will be able to contain the infection but when the CD4 count is low it will lead to disseminated infection.
Similarly, when (e.g. AIDS) the CD4 count is low enough it will lead to MAI aka MAC (Mycobacterium avium complex) infection.

 

[thehundredthone]

Hi all, so I'm finally starting to preview micro, path, and pharm before my 2nd year starts this fall. Hopefully this effort will make my 2nd year less painful.

My questions are:
1. So the reason you may expect low CD4 T cell count is b/c M. tuberculosis is an intracellular pathogen that triggers CD8 cytotoxic T cells and TH1 helper that makes IFN which stimulates macrophage, right?
2. What do you meant by "disseminated?" How does this make low CD4 count?
3. What does MAI stand for? And why does that give low CD4 count?
4. I've always thought that CD8 cytotoxic cells kill virus infected cells. But do they also killed some of the intracellular pathogen infected cells by any chance? If not, why not?

Many thanks in advance.

Isn't understanding which way this really works what second year is for? If you absolutely have to, I think it would be a better idea to preview your second year using your textbooks, not review books, to avoid this kind of confusion.

Like Transposony said, it's the other way around. Correlation does not imply causality and all that. Disseminated means widespread (throughout the body) in medicine. Comes from the Latin "spreading of seed".

 

[Fatalis]

...............you were a MS1 the entire time!?
damn that explains a lot!!!!

 

[dyspareunia]

Hi all, so I'm finally starting to preview micro, path, and pharm before my 2nd year starts this fall. Hopefully this effort will make my 2nd year less painful.

FWIW I will be doing this over the summer as well (MS1 here). I'm going to look at textbooks (Robbins, CMMRS, and maybe Katzung pharm) and get a general idea of basic concepts though.

 

[notbobtrustme]

FWIW I will be doing this over the summer as well (MS1 here). I'm going to look at textbooks (Robbins, CMMRS, and maybe Katzung pharm) and get a general idea of basic concepts though.

If you really want to review path, buy Pathoma. Robbins sucks. It's probably the worst 40 bucks I spent, that book is garbage, unclear, and poorly organized.

CMMRS is a supplement; you can learn from it but having a good base beforehand really solidifies the content inside.

Pharm is worthless to pre-study for. It's just a phonebook to memorize wrt to drug names. If you put the time in during M2 year, it will not be a problem at all. There are very few concepts in pharmacology, but a whole lot of information to hold.

That said, I still think that studying M2 material before M2 starts is very low yield. Enjoy that last summer, you won't get anymore time off like that every again.

 

[Fatalis]

If you really want to review path, buy Pathoma. Robbins sucks. It's probably the worst 40 bucks I spent, that book is garbage, unclear, and poorly organized.

CMMRS is a supplement; you can learn from it but having a good base beforehand really solidifies the content inside.

Pharm is worthless to pre-study for. It's just a phonebook to memorize wrt to drug names. If you put the time in during M2 year, it will not be a problem at all. There are very few concepts in pharmacology, but a whole lot of information to hold.

That said, I still think that studying M2 material before M2 starts is very low yield. Enjoy that last summer, you won't get anymore time off like that every again.

i agree with the last point 100%
pathoma is really good. It is still nice to have robbins to refer to if you really dont understand something but ya pathoma puts things together nicely
for micro look into getting picmonic, it really helps
and ya dont even touch pharm for now. I cant even remember some of the drugs i studied 2 weeks ago lol

 

[dyspareunia]

If you really want to review path, buy Pathoma. Robbins sucks. It's probably the worst 40 bucks I spent, that book is garbage, unclear, and poorly organized.

CMMRS is a supplement; you can learn from it but having a good base beforehand really solidifies the content inside.

Pharm is worthless to pre-study for. It's just a phonebook to memorize wrt to drug names. If you put the time in during M2 year, it will not be a problem at all. There are very few concepts in pharmacology, but a whole lot of information to hold.

That said, I still think that studying M2 material before M2 starts is very low yield. Enjoy that last summer, you won't get anymore time off like that every again.

I was planning to do Pathoma as well, but I thought it might be too much of a "review" type thing. Is Pathoma useful for first-time learning?

I definitely hear the sentiment of enjoying the summer. I'm the type of person that benefits more from intermittent breaks rather than one long break.. so I'm hoping that I can get at least a little ahead during the summer (even just basic path/pharm knowledge) so that I can relax a little bit during certain MS2 blocks.

i agree with the last point 100%
pathoma is really good. It is still nice to have robbins to refer to if you really dont understand something but ya pathoma puts things together nicely
for micro look into getting picmonic, it really helps
and ya dont even touch pharm for now. I cant even remember some of the drugs i studied 2 weeks ago lol

Picmonic over FC? I use FC now, but haven't touched micro yet.

 

[MudPhud20XX]

FWIW I will be doing this over the summer as well (MS1 here). I'm going to look at textbooks (Robbins, CMMRS, and maybe Katzung pharm) and get a general idea of basic concepts though.

I actually also started pharm too. As Fatalis says you will forget quickly as I don't remember anything I learned from anatomy several months ago, but I do think it is better to start earlier to get the concept. The goal of our study shouldn't be memorizing details, it should be having an intuition and good understanding of medicine.

I joined SDN after I was so frustrated with my classes that they won't preparing for the board exam at all. I felt it was such a waste of time. So, I finished reviewing MS1 stuff with Kaplan just once (need to reinforce with UW and firecracker, which I intend to do during the summer.)

So I'm now using my spare time previewing MS2 stuff.

I haven't started pathoma, but based on what I hear form others, I agree with all that pathoma is way to go, but still kind of time consuming... This would be a nice strategy to do along with your class, but that's just my opinion. I am planning on previewing pathoma during the summer so I'm 100% prepared for the 2nd year.

I just started Goljan audio/note with his rapid review since we do cover some portion of path in our MS1 class. I find Goljan to be more intuitive. He is really good. He also combines everything from biochem to micro. No BS and straight to the point. I really like him. If I were you I would start with Goljan asap.

By the way, speaking of Goljan, for those wise guys out there, I have some questions:

Under rxn to injury theory page 60, it says as below:

"Atherosclerosis in an aorta - rxn to injury theory = injury to endothelial cells lining the elastic arteries and muscular arteries - what is injuring it? Ammonia in cig smoke, CO in cig smoke; so, poisons damage the endothelial cells; LDL damages it, and if its oxidized, it damages it worse; viral infections damage it, too. Chlamydia pneumoniae (2nd MCC atypical pneumoniae); pts with MI - most had Ab's against Chlamydia pneumonia, homocysteine - all these things damage endothelial cells"

So he is basically saying that similar shxt happens in atypical pneumoniaea just like in rhematic fever with group A strep (forming type II hypersensitivity)?

So you can get MI from C. pneumoniae???

Many thanks in advance.

 

[Fatalis]

the thing is man, I gave you a hard time at the beginning bc I thought you were just too lazy to look up answers. But if you havent even taken these classes yet, it is no wonder why you can't answer these questions you pose [which are all good questions btw]. My suggestion, write down all these questions you have in a word document and as you learn the fundamentals in ms2 you will be able to answer these questions yourself. Sorry, but sometimes it is annoying. It is as if I were an undergrad in lets say comp sci and I was asking 4th yrs about concepts I havent been taught but more importantly will be taught/get a chance to learn about in due time!
I understand how important the boards are but like everything just take it as it comes. Focus on your classes for now.
I am sure some SDN people are gonna flame me for saying this, but it is just my opinion

 

[Apoplexy__]

So he is basically saying that similar shxt happens in atypical pneumoniaea just like in rhematic fever with group A strep (forming type II hypersensitivity)?

So you can get MI from C. pneumoniae???

Short answer: No.
The reaction to injury theory is relatively poorly developed, especially when it comes to the role of microbes. I would basically forget trying to learn anything regarding the role microbes play in poorly characterized inflammatory states (IBD, atherosclerosis, sarcoidosis, etc...these all have some sort of poorly established conjecture that microbes may play a role in the pathogenesis).

But even IF C. pneumoniae and similar microbes had a role in atherosclerosis, I don't think they know whether it's direct damage or Type II HS like you're asking. Again, super low-yield concept and poorly understood in modern medicine. You certainly would not say that you can get MI from C. pneumoniae.

I agree with Fatalis about trying to review board-relevant material that you've already gone over in class as opposed to learning ahead of your class; you can still board prep this way and you'll avoid the weak framework and subsequently poor memory-logging of learning ahead. Either way though, I'm psyched for your MS2 future. You're going to absolutely kill the boards; if not for the knowledge you've gained through this studying you've been doing, then through your crazy work ethic.

 

[Transposony]

I have to say that many of my concepts are clearer and learned so much new about topics thought I knew thanks to MudPhud20XX's postings.