Prep for USMLEPrep for USMLE Forum
   Forum    Step 1  Step 2 CK Step 2 CS Step 3  Match  IMGs Resources Search






Previous Topic | Next Topic  Kaplan Q 




 
Kaplan Qbank USMLE



Author15 Posts
  #1

Hmmmm..... what do yo think?


___________________
Prioritize & simplify.

  #2

A

___________________
Forum Elite, But Step 2 Newbie....

  #3

No, someone else, please with an explanation.

___________________
Prioritize & simplify.

  #4

then its E. i say so by ruling out other options coz it cant be Ig or immune complexes

___________________
Forum Elite, But Step 2 Newbie....

  #5

Well that what Kaplan book says, but if you have a Big Robbins (Pathologic basis of disease 7 ed. ) and read chapter on Myasthenia Gravis, you would be surprised. ( Page 1344)

It's not E.


___________________
Prioritize & simplify.

  #6

B??

  #7

Yes, It's B.

___________________
Prioritize & simplify.

  #8

It is B.. Autoimmune destruction of postsynaptic ACh receptors; MG

  #9

I'm wondering, is there any destruction or it is just a blocking antibody?
I think It is TypeII HSR but noncytotoxic.
If you check on Kaplan Medical Note Book Immunology page 445 table II-13-7 it is clearly written that there is no comlement or effector cells contripution..
I quess the true answer is not there in the choices and they made a mistake, but at the end it is the Best answer we are looking for and we can say B as it is the nearest to truth although it is far away..

If I'm wrong.. would any one kidly correct me.

___________________
keep going.. as the GOING gets TOUGH, the TOUGH gets GOING.. keep going..

  #10

I checked out and I think it is incomplete table that I mentioned be4 and the Complement activation is implicated in the pathogenesis od Myesthenia Gravis.. It is B the best and correct answer, as the blocking antibodies also activate the complement and form MACs and destruction.
any additions or corrections are appreciated.

___________________
keep going.. as the GOING gets TOUGH, the TOUGH gets GOING.. keep going..

  #11

good question GG anybody cud fall for trap whether block or MAC at ach receptor.thanks for sharing!but i chose b when did it wink

  #12

GG , you means kap give wrong answer , then u better write to them . Since I am not having time now adays , so in Qs I might rush , if wrong , will read explaination instead of go to big text , but are we all sure any texts or mid size books or any are right for sure.
Now a days , what disturb me alot is , like FA , KME , kap LN , RR path etc almost all famous books have error but we never know until we discuss here or with frds or found the error on line in other forums or some here .
But now ur saying it Q banks or kap Qs have error too , so how abt UW , chnaces are error will b there too. God help us, have mercy , who will have time to go for every qs, notes , books to recheck with big texts , even , is the big texts are error free 100% at all , like God we said in RR path is not error free , so did Fa as bible [ God for st 1] also has tons of error .sadmad

Thanks GG , have more coming , so we will notice read every answer with the caution .

GL GL GL happy success study to us , all nodcoolnod

  #13

yes complement activation is implicated in myasthenia gravis but no complement activity in type 1 hypersensitivity......

___________________
i m not perfect but i wanna get close to it......

  #14

it looks like a case of myasthenia gravis and its antibody against Ach receptor so C

___________________
we expect others wishes, we dont miss something that we dont expect to have

  #15

"B" is correct.

Myasthenia gravis is a type II hypersensitivity. The antibody produced against acetylcholine receptors may either impair its ability to bind to acetylcholine (i.e. a blocking antibody), or it may cause destruction of the receptor by complement fixation or by inducing the muscle cell to eliminate the receptor through endocytosis.

Here is an excerpt from wikipedia:

In MG, the autoantibodies are directed most commonly against the acetylcholine receptor (nicotinic type), the receptor in the motor end plate for the neurotransmitter acetylcholine that stimulates muscular contraction. Some forms of the antibody impair the ability of acetylcholine to bind to receptors. Others lead to the destruction of receptors, either by complement fixation or by inducing the muscle cell to eliminate the receptors through endocytosis.

The antibodies are produced by plasma cells, that have been derived from B cells. These plasma cells are activated by T-helper cells, which in turn are activated by binding to acetylcholine receptor antigenic peptide sequences (epitopes) that rest within the histocompatibility antigens of antigen presenting cells. The thymus plays an important role in the development of T-cells, which is why myasthenia gravis is associated with thymoma. The exact mechanisms are however not convincingly clarified.

(Source: http://en.wikipedia.org/wiki/Myasthenia_gravis)












You don't have permission to post.




Login or Register to post messages in this topic





















Contact | Leaders | Disclaimer | Privacy

Copyright @ Prep for USMLE. All rights reserved.