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  #1  
Old 02-25-2012
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Arrow NBME 5 Block 3 discussion

Q42:

Why not E??? Why B???


Q47:

I think the answer is D. The end diastolic volume in the adult is greater which means LV is a bit more dilated. In Hypertrophy the end diastolic volume should be smaller.
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Quote:
Originally Posted by haga View Post
Q42:

Why not E??? Why B???


Q47:

I think the answer is D. The end diastolic volume in the adult is greater which means LV is a bit more dilated. In Hypertrophy the end diastolic volume should be smaller.

Qs 42 ans is B becoz Basal cell CA never metastases ... its locally invasive ...so wide excision and lymph node dissection is not the ans , since the size is only 2mm cryotherapy is best ....

Qs 47 yes EDV is increased but if you see the SV has increased and the heart rate is low so this can be achieved only by hypertrophy , in DCM there is Increase in EDP and EDV but decrease in SV and CO

in normal aging UW says there is decrease in Apex to base dimension but sigmoid shaped septum and myocyte atrophy may have increased EDV ...

Hey could you explain 16 .. did not get why IgG is low even after 2 months ??
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Hey could you explain 16 .. did not get why IgG is low even after 2 months ??
Ok this concept I picked up from Kaplan Qbank. I'm not sure if it's the right thing to apply here but it makes sense to me.

There are subclasses of IgG. IgG1 is the main form so it is not considered a subclass. Its deficiency would cause all IgG levels to drop. The true subclasses are IgG2, IgG3, and IgG4. Their deficiency would go unnoticed.

The trick here is knowing which IgG is responsible for a response against Polysaccharide antigens. IgG2 is the one that is produced as an antibody aginst polysaccharide.

Now since no IgG was formed in this question, I'm thinking that this child has IgG2 deficiency. All the other antigens in the list of answers would be specific for IgG1 response.
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Quote:
Originally Posted by haga View Post
Ok this concept I picked up from Kaplan Qbank. I'm not sure if it's the right thing to apply here but it makes sense to me.

There are subclasses of IgG. IgG1 is the main form so it is not considered a subclass. Its deficiency would cause all IgG levels to drop. The true subclasses are IgG2, IgG3, and IgG4. Their deficiency would go unnoticed.

The trick here is knowing which IgG is responsible for a response against Polysaccharide antigens. IgG2 is the one that is produced as an antibody aginst polysaccharide.

Now since no IgG was formed in this question, I'm thinking that this child has IgG2 deficiency. All the other antigens in the list of answers would be specific for IgG1 response.
No , this appears to be the ans , i found it on another forum .

Bacterial Polysacharide is "T-cell Independent Antigen"
which directly stimulate B-cells and cz "IgM response" ONLY.(or if there is any slight response of other Ig , that will be IgG3)

*T-cell Independent Ag are METABOLIZED by the body "SLOWLY" and tend to stay in the system longer as compare to T-cell Dependent Ag, which get metabolized "RAPIDLY"

and perhaps this is what explains the IgM response for the period of 2 months.

*Haptens are T-cell Dependent and "ONLY trigger immune response" when they are "CONJUGATED"----so say like if we gave Unconjugated hapten injection, which later become conjugated and form "Hapten-carrier Adduct"........this complex has to go thru processing by Ag-presenting cells(a T-cell DEPENDENT route).


Other examples of T-cell INdependent Ag:

-Bacterial Lipopolysacharide(LPS)
-Flagellar protein" Flagellin"
-Dextran

and they DO NOT produce Memory cells...and this is the reason we conjugate H.Influenza Capsular Polysacharide to a protein ,so that it can become T-cell Dependent and produce Memory cells.


also see pg no 73 in Kaplan humoral immunity chapter .
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ok thanks!!!
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Old 02-26-2012
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help with:

Q10

Q17: whats the diagnosis and is there anywhere i can read on these techniques? i dont even know when to use x-ray vs CT vs MRI etc etc

Q34: why not NE?

Q36

Q42
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Guys what are they asking in Q 32.I am not able to understand can someone explain it to me???
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Quote:
Originally Posted by mohitkmc View Post
Guys what are they asking in Q 32.I am not able to understand can someone explain it to me???
i totally guessed that question and got it right lol
all i know is R for S12 gave really high numbers (60s) for both, so i chose it lol

can you help me with the questions i posted above?
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Qs 10 such Qs about HR and Bp are ususally about NE or Epi

here you see that it Increases Bp so has alpha effect and reflex bradycardia so not much of Beta response

now after Y the BP becomes normal so alpha effect has been antagonised and the HR increases due to Beta 1 effect but since BP is Normal and has not decreased there is no Beta 2 effect so now you know it NE without Beta 2 effect and prazocin blocking alpha 1 so ans is C

Qs 17 ans is E , its a tension pneumothorax , a tall guy , young , rupture of apical subpleural bleb cause tension pneumothorax and the xray findings tell you a collapsed lung is seen , its a emergency , you dont need futher test but the first step is to puncture the pleura in the mid coastal line to relieve the pressure , we were taught this in final year didnt find it in the kaplan or FA

Qs 34 MDMA inhibits seritonin uptake , LSD acts as seritonin agonist and the patient is taking paroxetine plus seritonin syndrome symptoms

see this
http://en.wikipedia.org/wiki/Serotonin_syndrome

http://www.mdma.net/serotonin/serotonin-syndrome.html

Qs 36 blood stored has citrate which chelates calcium

Qs 42 ans is B becoz Basal cell CA never metastases ... its locally invasive ...so wide excision and lymph node dissection is not the ans , since the size is only 2mm cryotherapy is best ....
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Quote:
Originally Posted by mohitkmc View Post
Guys what are they asking in Q 32.I am not able to understand can someone explain it to me???

Ans is B , now you that streptomycin works on 30 S , so its either S12 or S5

now check S12 .... see them in a line when it says S means sensitive the value without streptomycin is 63 and with streptomycin is 41 .. this shows that the S12 was inhibited by streptomycin , now see it the same way for R resistant ... similarly check for S5 and you will find that only S12 values match for S and R not S5
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Quote:
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Qs 17 ans is E , its a tension pneumothorax , a tall guy , young , rupture of apical subpleural bleb cause tension pneumothorax and the xray findings tell you a collapsed lung is seen , its a emergency , you dont need futher test but the first step is to puncture the pleura in the mid coastal line to relieve the pressure , we were taught this in final year didnt find it in the kaplan or FA
i've seen the description "sharp line running parallel to the chest wall" in two questions now, what does that indicate?
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Originally Posted by Dr.NickRiviera View Post
i've seen the description "sharp line running parallel to the chest wall" in two questions now, what does that indicate?
collapsed lung ....
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collapsed lung ....
so that would point me towards which diagnoses? atalectasia kind of stuff? like emphysema, ARDS?
(sorry but i suck at respiratory)
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so that would point me towards which diagnoses? atalectasia kind of stuff? like emphysema, ARDS?
(sorry but i suck at respiratory)
Yes , in pneumothorax remember your clues are a tall young man , because tall men have larger incidence of subpleural apical blebs and smoking increases risk futher ... now the patient will present with acute dyspnea ... then they will definitely tell you the x ray findings becoz that confirms the diagnosis and doesnot need futher CT or MRI ... x ray will show you a lung border of the collapsed lung as its a tension pneumothorax and a hyperlucent area from the collapsed margin to the chest wall as it is filled with air ...

now your best step is the relieve the air trapped there which increases with every breath by puncturing the pleura in mid clavicular line 2 or 3 ICS ...
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Yes , in pneumothorax remember your clues are a tall young man , because tall men have larger incidence of subpleural apical blebs and smoking increases risk futher ... now the patient will present with acute dyspnea ... then they will definitely tell you the x ray findings becoz that confirms the diagnosis and doesnot need futher CT or MRI ... x ray will show you a lung border of the collapsed lung as its a tension pneumothorax and a hyperlucent area from the collapsed margin to the chest wall as it is filled with air ...

now your best step is the relieve the air trapped there which increases with every breath by puncturing the pleura in mid clavicular line 2 or 3 ICS ...
man, i really need to step my respiratory game up...
i barely understood half of what you said lol

thanks though

how do you recommend i study respiratory? goljan?
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Please, can someone explain the following:

Q1: The t1/2 is 4hrs (240-120ng). Then the level should fall below 10 after 5 t1/2 then why 16 hrs & not 20 hrs?

Q2: Why "You seem to be developing an alcohol problem. You need to quit drinking. I can refer you to the local chapter of AA"- Isn't this too confrontational?
Why not assess r/o suicide by asking him about the suicidal ideation?

Q31: Why Methacarbamol (muscle relaxant) and why not Amitryptilline? She seems to have vague non specific signs and symptoms aggravated by recent life events.

Thanks in advance.
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Q1 and Q2.... i got them wrong the same way u did...
Q31 - the pt has fibromyalgia.. symmetrical tender points on palation at lat condyles etc... long history aggravated by stressors.... treatment is methylcarbamol (guafenesin)
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Quote:
Originally Posted by drssbaz View Post
Please, can someone explain the following:

Q1: The t1/2 is 4hrs (240-120ng). Then the level should fall below 10 after 5 t1/2 then why 16 hrs & not 20 hrs?

Q2: Why "You seem to be developing an alcohol problem. You need to quit drinking. I can refer you to the local chapter of AA"- Isn't this too confrontational?
Why not assess r/o suicide by asking him about the suicidal ideation?

Q31: Why Methacarbamol (muscle relaxant) and why not Amitryptilline? She seems to have vague non specific signs and symptoms aggravated by recent life events.

Thanks in advance.
Hey l;et me tell you again that you have the wrong answers in the key i think. Chek the link i sent you!

1. answer is D

2. answer is C

31. I think its amytryptiline not mrthcarbamol!
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Q1 and Q2.... i got them wrong the same way u did...
Q31 - the pt has fibromyalgia.. symmetrical tender points on palation at lat condyles etc... long history aggravated by stressors.... treatment is methylcarbamol (guafenesin)
yes the patient has fibromyalgia but the treatment is amytriptiline!
Honestly i dont know what methylcarbamol is but guafenesin is an expectorant
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can anyone explain this?

Number 19. Ok i got the answer but in the question it says you would give the patient atropine too! whats the atropine for??? you already have tubocurarine antagonizing acetylcholine so why do you give them another anticholinergic??

Number 32. the best wild guess of my life which turned out to be correct.
I dont even get what they are trying to ask! Seems like a total WTF question to me

Number 33. i guessed meckel's but how come it didnt show up on the barium contrast study??
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Originally Posted by numbndumb View Post
yes the patient has fibromyalgia but the treatment is amytriptiline!
Honestly i dont know what methylcarbamol is but guafenesin is an expectorant
methylcarbamol is a crbamol of guaifenesin but doesnt produce guaifenesin in metabolism... yes guaifenesin is a expectorant... and yes alll of this is no yield... lol... but that was the ans in the key i had, so made a story around it.. thanks for the correction...
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Quote:
Originally Posted by numbndumb View Post
can anyone explain this?

Number 19. Ok i got the answer but in the question it says you would give the patient atropine too! whats the atropine for??? you already have tubocurarine antagonizing acetylcholine so why do you give them another anticholinergic??

Number 32. the best wild guess of my life which turned out to be correct.
I dont even get what they are trying to ask! Seems like a total WTF question to me

Number 33. i guessed meckel's but how come it didnt show up on the barium contrast study??
33- the pt was given a barium enema... it wud only go upto the ileocecal valve i guess... so meckel didnt show up...

32- cudnt make nothing of the Q given... it was a blind fact taught in med school... helped here...
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Originally Posted by ..sharma View Post
methylcarbamol is a crbamol of guaifenesin but doesnt produce guaifenesin in metabolism... yes guaifenesin is a expectorant... and yes alll of this is no yield... lol... but that was the ans in the key i had, so made a story around it.. thanks for the correction...
Did u also do NBME 5 recently? We can discuss it if you havent already gone through it
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i have gone thru it... had a tough time searching for the answers ... saw ur post and thought i cud help...
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Thumbs Up BETTER EXPLANATION TO ANSWER OF: NBME 5 Block 3 Q.16

Quote:
Originally Posted by Hitman View Post
No , this appears to be the ans , i found it on another forum .

Bacterial Polysacharide is "T-cell Independent Antigen"
which directly stimulate B-cells and cz "IgM response" ONLY.(or if there is any slight response of other Ig , that will be IgG3)

*T-cell Independent Ag are METABOLIZED by the body "SLOWLY" and tend to stay in the system longer as compare to T-cell Dependent Ag, which get metabolized "RAPIDLY"

and perhaps this is what explains the IgM response for the period of 2 months.

*Haptens are T-cell Dependent and "ONLY trigger immune response" when they are "CONJUGATED"----so say like if we gave Unconjugated hapten injection, which later become conjugated and form "Hapten-carrier Adduct"........this complex has to go thru processing by Ag-presenting cells(a T-cell DEPENDENT route).


Other examples of T-cell INdependent Ag:

-Bacterial Lipopolysacharide(LPS)
-Flagellar protein" Flagellin"
-Dextran

and they DO NOT produce Memory cells...and this is the reason we conjugate H.Influenza Capsular Polysacharide to a protein ,so that it can become T-cell Dependent and produce Memory cells.


also see pg no 73 in Kaplan humoral immunity chapter .

Bacterial vaccines eliciting only IgM response to:
"Bacterial Capsular Polyssaccharide".

Hib vaccine is a "Capsular polysaccharide and protein vaccine" T-cell dependent

IgM can be produced by B-cells (with or without T-cell help)

This Pt has: X-Linked Hyper-IgM Syndrome.

CD40L is map to X chromosome. Therefore, TH cells fails to express functional CD40L on their membrane and will thereby fail to give the costimulatory signal necessary for:

-The B-cell response to T-dependent antigens, so only IgM antibodies are produced.
-The B-cell response to T-independent antigens is unaffected.

Bacterial vaccines are :

1) DTap= C. diptheriae, C. tetani, B. pertusis. Toxoid vaccine

2) Hib= H. influenzae b. Capsular polysaccharide & Protein vaccine

3) MCV= N. meningitis. Capsular serotype vaccine

4) S. pneumoniae=
-Pediatric "PCV"= ( 7 capsular serotype & protein Vaccine )
-Adult "PPV" [pneumovax]= ( 23 capsular serotype, including resistant strains vaccine. )


Last edited by tatox; 06-18-2014 at 08:39 AM.
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