NBME CBSSA Form 2

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Pox in a box

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Keep all comments on this assessment (Form 2) within this thread. Giving questions and answers out in other threads is not helpful for people taking the CBSSA later.

Here's a FAQ because I'm sure there's going to be a dozen questions about what this exam is: http://www.nbme.org/PDF/sas.pdf

Here's the menu: http://www.nbme.org/programs/sas.asp

In summary, there are two assessment exams (both are 200 questions each and each one costs $45). It assesses your strengths and weaknesses (very loosely I might add) and gives you a "predicted" score.
 
Did anyone else find Form 2 harder, or was it just me? I took Form 1 sort of as a diagnostic before I started studying and got a 590. Two and a half weeks later after studying all sorts of crap I get a 520. 😱 Still a decent score, I know, but as I understand it, studying should make your score go up, not down. 🙄 So yeah, anyone else just find the Form 2 questions weird? I just remember thinking throughout that test, "Why is any of this relevant?" My test is on Friday, so hopefully everyone is right and you do way better than your Form 1 score :luck:
 
Wahoo07 said:
Did anyone else find Form 2 harder, or was it just me? I took Form 1 sort of as a diagnostic before I started studying and got a 590. Two and a half weeks later after studying all sorts of crap I get a 520. 😱 Still a decent score, I know, but as I understand it, studying should make your score go up, not down. 🙄 So yeah, anyone else just find the Form 2 questions weird? I just remember thinking throughout that test, "Why is any of this relevant?" My test is on Friday, so hopefully everyone is right and you do way better than your Form 1 score :luck:

My test is on friday as well. good luck!
 
Well, this thread needs some posts...

Questions I had:

1) What was the question stem describing in the patient with lesions on their scalp, face, groin and trunk - pemphigas vularis or bullous pemphigoid?

I picked the answer: "intraepidermal blister with suprabasal acantholysis"

2) What was the disease that the patient had with the question describing a healthy 32 y/o female with recurrent headaches, N/V, abdominal pain, and easy brusibilty. They then listed here labs (leukocytes 15,000, MCV 78, Platelets 30,000, and Hemoglobin 7 g/dL)?

I thought she might have a SLE pancytopenia-like thing going on? Not sure of her disease though. I picked the answer: SCHISTOCYTES

3) The child with Cretinism? Yikes! That didn't pop into my american-iodine-in-the-salt mind (even though, I know there is always the RARE sporadic inborn error of iodine metabolism). I kept saying "macroglossus - Down's syndrome and.... and... dang." I guessed right, but it was luck.

4) The infant with tonic-clonic seizures, ataxia, hypotonia, hairloss and rash (don't remember the question exactly - took test a couple of days ago). Then asked which vitamin (Biotin, B2, B6, B12, and C). I have no idea. Anyone?

Tough test. I was happy with my score, but I guessed a lot!

G-luck to all
-WISCite
 
Yes, I had questions too!
1. I think it was Bullous Pemphigoid? Because there was no mucocutaneous involvement? I don't remember my answer.
2. I thought she might have had TTP? I said schistocytes, because of the platelet count.
4. The infant with the crazy stuff happening was B6- I have written in my notes- convulsions, neuro symptoms and pellagra like symptoms. I guessed Biotin at the time however.
There were more I had q's on-I'll just pick a few though. Maybe these are easy and I just blanked or something.

How do you control otherwise well-controlled a-fib during exercise? I wasn't sure.

How do you slow the life of a peptide? enteric coating, decrease numbers of aa in the peptide, free amino group, free carboxy group, or substitute D for L aa?

If you give EPO to a diabetic with controlled htn on dialysis, what will be exacerbated? Renal insuffiency, DM, Htn, Osteitis Fibrosa Cystica, and I forget what the last answer choice is (actually , i have PN written in my notes and I don't know what it stands for). I arbitrarily picked hypertension.

Ah yes, and why don't women have catabolic responses to glucocorticoids? Increased metabolic clearance, increased steroid binding protein, increased steroid receptors, or increased steroid uptake mechanisms?
 
I had the same issues... wrote some of them down.
How do you control otherwise well-controlled a-fib during exercise? I wasn't sure.
- Options were: adenosine, lidocaine, nefedipine, propanolol, and quinidine. My roommate and I have hashed this one out as neither of us remembers the exact question... I think it said the person was well treated for A fib and wanted something for his stress and exercise fibrillations - so I picked metropolol. My roommate disagrees with how I remember the question though.

How do you slow the life of a peptide? enteric coating, decrease numbers of aa in the peptide, free amino group, free carboxy group, or substitute D for L aa?
- I picked substitue D or L, but I have no idea if that is right.

If you give EPO to a diabetic with controlled htn on dialysis, what will be exacerbated? Renal insuffiency, DM, Htn, Osteitis Fibrosa Cystica, and I forget what the last answer choice is (actually , i have PN written in my notes and I don't know what it stands for). I arbitrarily picked hypertension.
- Me too, I think it is HTN as it would increase hematocrit and viscocity. Can confirm the HTN though.

Ah yes, and why don't women have catabolic responses to glucocorticoids? Increased metabolic clearance, increased steroid binding protein, increased steroid receptors, or increased steroid uptake mechanisms?
-I put Increased Steroid Binding Protein.

Pharm is not my phriend,
WISCite
 
What did you guys put for initiating the talk on alcohol?

How much do you drink in a week?
What is your favorite drink?
Do you think you are a problem drinker?
 
I put: So how much do you drink in a week?

I got a right-sided star in Behavioral, so I think it is right.

As an aside, at my school we have been told to ask the question like this: "So, approximately how many drinks do you consume in one week?" Wait for a response. Then, "Would you say you drink a case or a fifth?"

The professor said that it will help identify the chronic drinker... but, it is Wisconsin and we drink a little more than others....

WISCite
 
Ok, so i took form 1 and got a score i was happy with 3 weeks ago....and today took form 2 and got 15 pts lower --eeks! i wanted a confidence boost, not a killer!

anyhoo, take my answers for what they're worth...(hopefully something!)

-for the alcoholic--i said 'how much do you drink in a week' (although the 'what is your favorite drink option made me laugh'..)

-i said enteric coating for the peptide just b/c wouldn't a peptide therapeutic last like a milisecond without?

-pemphigus vulgaris for the blister b/c didn't it say 'intraepidermal'? i think bullous is at the epidermal junction but i agree about the mucocutanous involvement..

-for the female pt with the headaches and labs, i said shistocytes b/c i was thinking along the lines of TTP (the 'FAT RN' mneumonic)

-afib/exericse--didn't know, stared at for a long time i remember trying to figure out what was going on. can't remember my answer

-what was the kidney image? pt who came in w/ hematuria, died in hospital after losing some kindof motor or sensory function (eg stroke)
i think i said renal cell CA and don't remember the other options...maybe renal infarct, polycystic kindey disease ithink...honestly, i can't see anything wrong with kidneys unless they have big ole cysts so i ruled that out.


did you guys take form a also?
 
KB
I said, How much do you drink in a week? Seemed the least judgmental of the bunch.

WISC-ite
I also put the substitute D for L aa for the same reason- I had no clue.
I was thinking along the same line for the htn with the viscosity and such, although I thought my brain was operating as a separate entity at the that point.
I put increased steroid binding receptors for no reason though. Agreeing on 2/3 isn't horrible though!

What about the kid who was born with (gulp!) no limbs? It was a mutation for FGR controlling either apoptosis, differentiation, epithelial and mesenchymal conversion, or proliferation. I think I said differentiation.

Ok, one more, I can't stop. Bilateral movement of the external oblique controls what movement of the vertebral column? Extension, Flexion, Lateral flexion, rotation. After trying to flex my external oblique, I decided flexion.
 
WISC-ite said:
I put: So how much do you drink in a week?

I got a right-sided star in Behavioral, so I think it is right.

As an aside and not to to make any jokes about alcoholism, at my school we have been told to ask the question like this: "So, approximately how many drinks do you consume in one week?" Wait for a response. Then, "Would you say you drink a case or a fifth?"

The professor said that it will help identify the alcoholics... but, it is Wisconsin and we drink a little more than others....

WISCite

Thanks

What did you guys put for the neonate with a heart murmur. What to do.

Tell the parents and examine child again
Tell the parents and get a cardiology consult

Also what about they guy that went into ketoacidosis? Cough Syrup, Dehydration, Failure to take insulin, Infection?


How do you guys handle the child development questions? There was a question on there. I'dont remember, just 100 word vocabulary.
 
jojo14 said:
KB
I said, How much do you drink in a week? Seemed the least judgmental of the bunch.

WISC-ite
I also put the substitute D for L aa for the same reason- I had no clue.
I was thinking along the same line for the htn with the viscosity and such, although I thought my brain was operating as a separate entity at the that point.
I put increased steroid binding receptors for no reason though. Agreeing on 2/3 isn't horrible though!

What about the kid who was born with (gulp!) no limbs? It was a mutation for FGR controlling either apoptosis, differentiation, epithelial and mesenchymal conversion, or proliferation. I think I said differentiation.

Ok, one more, I can't stop. Bilateral movement of the external oblique controls what movement of the vertebral column? Extension, Flexion, Lateral flexion, rotation. After trying to flex my external oblique, I decided flexion.


jojo--
for the kid w/out limbs (i know!!) i said differentiation, though i was also wondering about apoptosis...i know that comes into play with digits, but i wasn't sure.

bilateral movement of the ext obliques--I said rotation, and looking in moore's i saw a chart that said 'compress and support abdominal viscera, flex and rotate trunk'. so i think that rules out NONE of those answer options.....
I also did the 'flex my own' test and decided that i need to work out more.
 
The kidney patient I wondered about. I thought maybe polycystic kidney disease because of the Berry aneurysm connection, but I didn't know if APCKD could present with red cell casts. (weren't there casts? I can barely remember)

I also said tell the parents and get a consult because it said it was benign in up to 50% of patients. I figured that meant it was terrible in the other 50%, so I called cardio to be sure.

I did take form 1 and I scored 40 points higher on form 2, which I was obviously happy about, but I have heard that form 1 is more like the real thing so it all probably means nothing.
 
guarana
- I said renal infarct as the kidney had a small pale ischemic region near the top of the image - wasn't sure though, but the question implied the patient then had a stroke, so I thought the lady was throwing chunks from her valve.

Kluver_Bucy
- I said tell the parents and re-examine in 24 hours. I was stuck, but I reread the question stem and they said the condition was transient in 50% or kids. So, I guessed that they wrote transient to make us pick the non-cardiology consult answer.
-Awesome Username by the way.

Anyone have a clue about the question about the lady with pain and erythema on sun-exposed area with bullae? She had a reaction to methylparaben used in meds as a preservative. The options were mostly things I had never heard of (Avobenzone, Bensophenones, p-Aminobensoic acid esters, cinnamates, and salicylates). Ideas?
 
I said give the parents the info w/ a cardio consult also, b/c I think truth-telling is probably a good way to go with these q's

This might be a stupid question, but what did you guys say about the infant with ambiguous genitalia (or enlarged clitoris), what would you expect on biopsy of the adrenals. I went back and forth, would it be hypo or hyperplasia?? i mean, you would have no feedback inhibibtion if you were 21-OH deficient, but then those regions of the adrenals would be hypoplastic. but then everthing would be shunted towards androsterone synthesis, so wouldn't that be HYPERplastic?
 
WISC-ite, I said PABA esters, because PABA was the only thing I knew was in sunscreen for sure. Probably not the best way to go about it.

I said hyperplasia, as 21-0H deficiency is classified under the congenital adrenal hyperplasias.

What about the "what is needed for ciliogenesis" question? Answers were Biogenesis of added mitochondria (which I picked), chromosomal DNA, glycosylations in Golgi, multiplication of centrioles, and synthesis of cytokeratin.
 
WISC--
I haven't looked it up but I chose PABA sunscreens as the ones to avoid just b/c that is the only one I've heard of. I had a friend who had allergic reactions to sunscreens and she went far and wide to search for good PABA-free products. also, I was thinking along the lines of sulfa drugs...
 
WISC-ite said:
guarana
- I said renal infarct as the kidney had a small pale ischemic region near the top of the image - wasn't sure though, but the question implied the patient then had a stroke, so I thought the lady was throwing chunks from her valve.

Kluver_Bucy
- I said tell the parents and re-examine in 24 hours. I was stuck, but I reread the question stem and they said the condition was transient in 50% or kids. So, I guessed that they wrote transient to make us pick the non-cardiology consult answer.
-Awesome Username by the way.

Anyone have a clue about the question about the lady with pain and erythema on sun-exposed area with bullae? She had a reaction to methylparaben used in meds as a preservative. The options were mostly things I had never heard of (Avobenzone, Bensophenones, p-Aminobensoic acid esters, cinnamates, and salicylates). Ideas?

I heard it is pABA.

What about the kid with an earache, tugging his ears I think. typanic canal and membrane look normal? Serous, Purulent Otis media, Otitis Exteran, Auditory tube obstruction.
 
Kliver--
I was thinking an otitis media, except the TMs were clear but i couldn't rationalize the other options (how does one obstruct one's eustacian tube? did i miss that day?)

So I said 'serous' otitis media. I'm not confident at all with my answer though, I'd be curious to hear what others said.....
 
Serous? Wasn't purulent, otitis externa you should be able to see, and I picked serous over auditory tube obstruction. This is probably a dumb q, but is the auditory tube the same as the eustachain tube? I guess that could happen if it is, because that's how most ear infections start out. Maybe that's the answer.
 
Sorry, but it said obstruction huh. Maybe not. Maybe it was serous.
 
jojo14 said:
Serous? Wasn't purulent, otitis externa you should be able to see, and I picked serous over auditory tube obstruction. This is probably a dumb q, but is the auditory tube the same as the eustachain tube? I guess that could happen if it is, because that's how most ear infections start out. Maybe that's the answer.

I wouldn't know where to start with those ear questions.

what about they guy that went into ketoacidosis? Cough Syrup, Dehydration, Failure to take insulin, Infection? Didn't the question say he uses insulin?
 
Oh yeah, I said infection, because it puts a stress on the body and I figured maybe his insulin dosage couldn't handle it.
 
jojo14 said:
Oh yeah, I said infection, because it puts a stress on the body and I figured maybe his insulin dosage couldn't handle it.

Is this in any book, I've never heard of infection can decrease efficacy. I'm just so lost, any kind of help would be appreciated.
 
for the ketoacidosis guy--
was 'infection' one of the options? if so, I think I picked that (I think I remember that the increased metabolism involved in an acute infection can often drive a diabetic into DKA..)

ahhh, it's all becoming a blur already. and i wasn't even stressed out taking this one! i wonder what the real thing is going to be like.

did you guys think it was odd that the IL-2/cyclosporin/tacrolimus/OKB-whatever it is came up more than once? definitely need to look at that!
 
OK, in my edition of First Aid, it says under the DKA section: One of the most important complications of type I DM, usually due to an increase in insulin requirements from an increase in stree (e.g. infection).

I'm glad you made me look it up! I just picked it because the one patient I have ever had with diabetes was diagnosed with it after he had an episode of DKA after a recent illness. Keep in mind that this is usually how little kids with DMI present with the diagnosis- they got a cold/flu and started peeing/drinking/sleeping like crazy!
 
Yes, thank you that totally freaked me out. I reviewed it yesterday but I still am clueless on those drugs. Any hints for remembering stuff?
 
Thanks. You are right. First Aid packs a punch. Every word in the high yield section is high yield. Unbelieveable. Not many people would have noticed that in first aid. No wonder people say read that book many times.
 
Wahoo07 said:
Did anyone else find Form 2 harder, or was it just me? I took Form 1 sort of as a diagnostic before I started studying and got a 590. Two and a half weeks later after studying all sorts of crap I get a 520. 😱 Still a decent score, I know, but as I understand it, studying should make your score go up, not down. 🙄 So yeah, anyone else just find the Form 2 questions weird? I just remember thinking throughout that test, "Why is any of this relevant?" My test is on Friday, so hopefully everyone is right and you do way better than your Form 1 score :luck:

I thought they were about the same. Form 2 seemed to be more focused on pathology in my opinion. There were only a couple of behavioral science, anatomy, and biochemistry questions. It was very heavy in pathophysiology.
 
Kluver_Bucy said:
Is this in any book, I've never heard of infection can decrease efficacy. I'm just so lost, any kind of help would be appreciated.

This is coming from left field but I had the same thought process during the exam. I have no idea why but it was a good immediate hunch before I saw the answer choices.
 
Pox in a box said:
This is coming from left field but I had the same thought process during the exam. I have no idea why but it was a good immediate hunch before I saw the answer choices.

Thanks, it is good to know that it wasn't just me. I just feel so overwhelmed. My score on the form was a 390. I still have 3 weeks until my exam day but feel like I don't know anything. I don't know what I would be like if it wasn't for kind people like omarsaleh and samyjay helping me. When are you taking your exam?
 
Kluver_Bucy said:
I wouldn't know where to start with those ear questions.

what about they guy that went into ketoacidosis? Cough Syrup, Dehydration, Failure to take insulin, Infection? Didn't the question say he uses insulin?

For the kid with the seizures and the vitamin deficiency...I think it might be biotin...because they said the patient had "multiple carboxylase deficiency"...isn't biotin a cofactor for carboxylations? (FA 2005 p.163) Also, the kid had hair loss and dermatitis... biotin deficiency causes hair loss and dermatitis...i'm not sure if B6 deficiency causes hair loss.

A few questions for you all:

1. The question about a patient 2 mos post Renal transplant with increasing dyspnea...xray shows interstitial infiltrate. They showed a lung Bx pic...looked like inclusion bodies to me...was it CMV?

2. C. perfringens evades destruction by neutrophils how?
a. Damaging neutrophil membranes by means of a membrane-damaging toxin
b. Preventing contact with neutrophils by means of a polysaccharide capsule
c. Preventing phagocytosis by disruption of neutrophil actin polymerization
d. Survival in the cytoplasm of a neutrophil
e. Survival in the phagosome of a macrophage

Are they trying to get at the lecithinase toxin from C. perfringens damaging the membrane? If so...that's pretty darn picky.

3. This was a confusing one:
How to distinguish central diabetes insipidus from nephrogenic diabetes insipidus?
a. Injection of ADH (vasopressin)
b. Injection of hypertonic saline
c. Injection of insulin
d. Water deprivation
e. Water loading

Here is a quote from emedicine:
"The definitive diagnostic study is the water deprivation test, which can be used both to confirm the diagnosis and to distinguish between CDI and NDI by response to a vasopressin analogue."
Isn't that saying that to distinguish between the two, use the water deprivation test and then test the response to vasopressin...doesn't that encompass both a) and d)?

I also was confused with that otitis media question...I think most of us think it's serous otitis media (I put that too), but isn't serous otitis media CAUSED by obstruction the eustachian tube (both of those were answer choices)...<shrug>

So according to my score report, I need to improve my behavior...who would've thought?? 😛

Thanks in advance for your input...good luck everyone!
 
Long Dong said:
How do you test concentration?


yeah! what the heck was that one? i didn't even know how to look that up!

i forget the exact answers, but one involved repetition so i did NOT say that.

(as an aside--is concentration even a definitive medical term? i mean, there is memory, reasoning, intellegence, etc....but do you ever write up that someone seems to have severe deficits in....concentration?)
 
for the question regarding the newborn with the heart murmur, I'm pretty sure the right answer is tell the parents, check again in 24 hrs. the author of BRS Behavioral Science kept emphasizing over and over that getting a consult will never be the right answer on the boards. I got a asterik all the way at the right with no bar on my evaluation for behavioral science, so i'm not sure if that means i got them all right or not.

i put auditory tube obstruction for the kid with the tympanic membrane that wouldn't move. otitis media just didn't seem right to me, but i really don't know.

I think I put lidocaine for the arrhythmia question. I looked it up in Lippincotts, and they say that quinidine is suppresses arrhytmias caused by normal automaticity while lidocaine suppresses arrhythmias from abnormal automaticity. I thought a. fib. would fall into the latter category.

I thought form 2 was harder than form one although I did 8 points higher (or 50 points higher) on form 2, so it's just tough to tell i guess.
 
Took the test today...overall not too bad. I did much better than form 1. Here are some answers that i think are right. Seems like the tests are more about figuring stuff out than they are about remembering minute details...

1) YEs CMV - big owl eye cells
2) Yes lecinthinase damages membranes of ALL cells
3) the answer is ADH injection - water deprivation by itself doesnt distinguish between the two
4) otitis media question: the answer is eustacian tube blockage because there was something in the stem about increasing pharyngeal pressure doesnt move tympanic membrane - this means that the nasopharynx is not connected to middle ear - i actually watched a surgery for this very reason a little while ago where they put a tube through the tympanic membrane to prevent pressure buildup in the middle ear. I think its a common condition in kids as well as adults...but you best look it up to be sure.
5) for the exercise and stress arrythmia, you have think about what exercise and stress have in common which is adrenergic stimulation so i put beta blocker.

Anybody get the sunscreen question? what the hell was that?
 
for the sunscreen one check the page before, i think a few of us were thinking PABA but no one really was certain..
 
geromine said:
Anybody get the sunscreen question? what the hell was that?

So the question was saying something about a woman who had "major positive reactions" to methylparaben...which of the following sunscreens is contraindicated...

here is what i found here:
http://www.osha.gov/dts/chemicalsampling/data/CH_254445.html

This page is for methylparaben...
"Health Effects: Allergic contact dermatitis (uncommon); skin sensitization (rare).

Affected organs: Skin

Notes: 1) Readily and completely absorbed through the skin or after ingestion, hydrolyzed to para-hydroxybenzoic acid, and metabolites are rapidly excreted in the urine. 2) May show cross-sensitivity in people allergic to local anesthetics that are metabolized to para-aminobenzoic acid."

There we go...PABA...pretty random question if you ask me...
 
thanks... I still cant figure out why they would ask that questions.

did anyone get the kid with abdominal mass with "binucleate cells" - it sounded like RS cells but the age and the abdominal mass didnt really work with it so i went with burkitt but i cant seem to find anything about binucleate cells on the web for burkitt so im thinking maybe it was hodgkins afterall. Any ideas?
 
geromine said:
thanks... I still cant figure out why they would ask that questions.

did anyone get the kid with abdominal mass with "binucleate cells" - it sounded like RS cells but the age and the abdominal mass didnt really work with it so i went with burkitt but i cant seem to find anything about binucleate cells on the web for burkitt so im thinking maybe it was hodgkins afterall. Any ideas?

Actually, I think the question said the kid had a mediastinal mass (rather than an abdominal mass) with firm bilateral cervical lymph nodes...I think that makes it more likely to be Hodgkins, no?
 
Long Dong said:
How do you test concentration?

I think this was counting backwards or doing some kind of adding or subtractring. I remember learning something like this in psych? Not sure tho.
 
Just took the NBME 2 exam. Personally thought it was much harder than the 1st exam, even though i did a lot better. Go figure. Anyways, wanted to throw out some questions to see if anyone out there knew what the right answer was.

-Which of following immunosuppressive drugs acts be selectively binding to epsilon chain of T lymphocyte antigen-receptor complex?
-antilymphocyte globulin
-anti-TNF-alpha monoclonal antibody'
-azathioprine
-corticosteroids
-cyclosporine
-OKT3 monoclonal AB

I picked OKT3, not sure though, anyone heard of the Epsilon chain before?

Which part of the brain is responsible for Deja vu??

A eukaryotic protein that's non-membrane assosciated, glyclosylated, disulfide-linked dimer in the mature form, generally found where?
-cytoplasm
-extracellular space
-mitochondrial matrix
-nuclear matrix
-nuclear pore

I had no idea on this one, i picked extrcellular space.

What about that lady you got chest pain after walking up a flight of stairs at her work. She took some medication so she could carry on. It asked what the medication did

-decreased afterload
-decreased preload
-increased after and preload
-increased preload
-incerased contractility

I put decreased afterload, but wasn't sure. It sounded like stable angina to me, wouldn't you take nitrates? What does that do exactly in reference to the above choices? I guess you could also take beta blockers. Not sure. Anyone?

Thanks!
 
Ologist said:
Just took the NBME 2 exam. Personally thought it was much harder than the 1st exam, even though i did a lot better. Go figure. Anyways, wanted to throw out some questions to see if anyone out there knew what the right answer was.

-Which of following immunosuppressive drugs acts be selectively binding to epsilon chain of T lymphocyte antigen-receptor complex?
-antilymphocyte globulin
-anti-TNF-alpha monoclonal antibody'
-azathioprine
-corticosteroids
-cyclosporine
-OKT3 monoclonal AB

I picked OKT3, not sure though, anyone heard of the Epsilon chain before?

Which part of the brain is responsible for Deja vu??

A eukaryotic protein that's non-membrane assosciated, glyclosylated, disulfide-linked dimer in the mature form, generally found where?
-cytoplasm
-extracellular space
-mitochondrial matrix
-nuclear matrix
-nuclear pore

I had no idea on this one, i picked extrcellular space.

Thanks!

Epsilon chain is part of CD3, which OKT3 targets.

As for the eukaryotic protein, it is describing an immunoglobulin, so it would be found in the extracellular space.

Your friendly immuno nerd.
 
Ologist said:
A eukaryotic protein that's non-membrane assosciated, glyclosylated, disulfide-linked dimer in the mature form, generally found where?
-cytoplasm
-extracellular space
-mitochondrial matrix
-nuclear matrix
-nuclear pore

I had no idea on this one, i picked extrcellular space.

What about that lady you got chest pain after walking up a flight of stairs at her work. She took some medication so she could carry on. It asked what the medication did

-decreased afterload
-decreased preload
-increased after and preload
-increased preload
-incerased contractility

I put decreased afterload, but wasn't sure. It sounded like stable angina to me, wouldn't you take nitrates? What does that do exactly in reference to the above choices? I guess you could also take beta blockers. Not sure. Anyone?

Thanks!


sup all, took the 2nd one...it was harder.....it was totally like a skip lesion of hard questions. Some were pretty straight forward and then it was hard, and then it was easier, and then it was hard. Lol, anyone else feel the same way.

for the two questions above.

1) I believe the protein would be an "immunoglobulin" aka Ab that has been secreted into the "extracellular space". the molecule of a Ig is linked together by disulfide bonds.

2) She sounds like she has stable angina which is probably relieved by her use of nitrates (NG, isosorbide dinitrate, etc). Nitrates tend to be venodilators vs your arteriodilators (hydralazine). Nitrates affect teh venous system so we're talking about venous return and pre-load.

Based on that you could answer the question; but here's a little longer explanation to make it stick.

Nitrates--> VD--> Increased radius--> decreased resistance--> decreased pressure aka DBP (based on the formula Q=P/R; and since this is a closed system Q doesn't change) --> increased venous return --> increased pre-load.

While nitrates can dilate arteries, I think that the increased pre-load would have been the better answer. It allows her hard to accomodate more volume to keep up with her increased myocardial o2 demand.

hope this helps and g'luck everyone....

ucb
 
ucbdancn00 said:
sup all, took the 2nd one...it was harder.....it was totally like a skip lesion of hard questions. Some were pretty straight forward and then it was hard, and then it was easier, and then it was hard. Lol, anyone else feel the same way.

for the two questions above.

1) I believe the protein would be an "immunoglobulin" aka Ab that has been secreted into the "extracellular space". the molecule of a Ig is linked together by disulfide bonds.

2) She sounds like she has stable angina which is probably relieved by her use of nitrates (NG, isosorbide dinitrate, etc). Nitrates tend to be venodilators vs your arteriodilators (hydralazine). Nitrates affect teh venous system so we're talking about venous return and pre-load.

Based on that you could answer the question; but here's a little longer explanation to make it stick.

Nitrates--> VD--> Increased radius--> decreased resistance--> decreased pressure aka DBP (based on the formula Q=P/R; and since this is a closed system Q doesn't change) --> increased venous return --> increased pre-load.

While nitrates can dilate arteries, I think that the increased pre-load would have been the better answer. It allows her hard to accomodate more volume to keep up with her increased myocardial o2 demand.

hope this helps and g'luck everyone....

ucb

I may be wrong but I belive the way nitrates reduce O2 demand is by decreasing preload. Venodilating the venous system prevents return of blood to heart and so it has less to deal with. Nitrates also vasodilate the coronaries which helps deliver more O2 to meet the demand.
 
So I had bunch of questions after taking this one; if anyone could share their thoughts - that would very helpful and much appreiciated 🙂

1. A 48-year-old man comes to his physician because his wife noticed that his right pupil is "small." Physical examination shows that the right pupil is constricted and does not react to light. His left pupil is normal. These findings are most likely due to a lesion involving which of the following structures on the right?
A ) Cervical spinal cord
B ) Frontal eye fields
C ) Lateral geniculate nucleus
D ) Optic tract
E ) Visual cortex

While B-E would cause defects the man doesn't have (contralat hemiopsisa etc.) Yet I thought to cause Horner's, you had to lesion the sympathetic chain somwhere. Where exactly could you lesion the spinal cord to cause this?

2) Osteoporosis (T8 compression fracture, postmenopausal women losing height)
bone biposy of iliac crest shows:
- cysts filled w/ fibroblasts and giant cells
-disorderly osteoblastic and osteoclastic activity
- thin trabeculae w/ low osteoclastic activity

I agree w/ thin trabeculae but I thought OP had high Oclast activity

3) response to a systemic bacterial infection w/ fever and shaking chills is due to
- hypothalmic repsonse to leukocytosis
- release of leukocyte cytokines into circulation
(hypothal abscess, damaged hepcyte frags released, leukocyte inflm of hypothal were the other choices)

4) A 15-year-old girl has had a sore throat and temperatures to 37.7 C (100 F) for 3 days. Physical examination shows erythematous pharyngeal mucosa and cervical lymphadenopathy. Leukocyte count is 12,000/mm3 with 60% lymphocytes. A slide agglutination test is positive for antibodies against Epstein-Barr virus. This virus is most likely to replicate initially in which of the following cells?
A ) Peripheral blood B lymphocytes
B ) Peripheral blood monocytes
C ) Peripheral blood T lymphocytes
D) Pharyngeal B lymphocytes
E ) Pharyngeal monocytes
F ) Pharyngeal T lymphocytes

Mono first must invade through the pharynx but does replication begin in the B cells of peripheral blood (thats what I went with)

5) A stressed myocardial cell that has no calcium gradient across its plasma membrane most likely has undergone which of the following processes?
A ) Abortive mitosis
B ) Adaptation
C ) Cell death
D ) Repolarization
E ) Reversible cell injury

cell death?

11) 95% obstructed L renal artery wild mild compensatory hypertrophy on the R kidney. what happens? Would you see
- decreased renin and decreased Angiotensin 1 w/ loop diuretic
- increased renin after ACE Inhibitor

12.) Alveolitis with interstitial edema, inflammatory cell accumulation, and type II epithelial cell hypertrophy and hyperplasia is believed to be an early and central event in the pathogenesis of
A) anthracosis
B) asthma
C) centriacinar emphysema
D) chronic bronchitis
E) pulmonary fibrosis

Thanks so much!
 
Every single last one of these were on my list to look up!

1. Here is a cool animation on pupillary constriction.
http://medstat.med.utah.edu/kw/hyperbrain/anim/reflex.html
The answer was probably optic tract from what I looked up. If so, I got that wrong though.

2. Baby Robbins says thin trabeculae, but it also says "slowing of osteoblastic function and increased osteoclastic activity," so I suppose that could be "disorderly."

3. The FA chart shows IL-1/IL-6/TNF-alpha --> Hypothalamus --> Increased body temperature. Since IL-1 & TNF-alpha, cytokines, are secreted by macrophages which are leukocytes, and affects hypthalamus... who knows.

4. From Emedicine: "EBV infects the B cells in the oropharyngeal epithelium. Circulating B cells spread the infection throughout the entire reticular endothelial system (RES), ie, liver, spleen, and peripheral lymph nodes. EBV infection of B lymphocytes results in a humoral and cellular response to the virus. The humoral immune response directed against EBV structural proteins is the basis for the test used to diagnose EBV infectious mononucleosis. However, the T-lymphocyte response is essential in the control of EBV infection; natural killer (NK) cells and predominantly CD8+ cytotoxic T cells control proliferating B lymphocytes infected with EBV."
From other things I've scanned, it seems to replicate in the pharyngeal area.

5. I believe it's cell death. It seems that calcium enters the cell right before cell death, and CCB's can counteract that. but don't quote me.

11. ACE inhibitors normally increase renin because of the decreased Renal Blood flow and the feeback mechanism. Renal artery stenosis alone increases renin (which is why it causes HTN) due to the decreased blood flow. ACEI are dangerous for a patient in renal artery stenosis because it can decrease blood flow even more than the stenosis has, and can send the patient into acute renal failure (high BUN, Creatinine, etc.) So my thinking is the answer is increased renin.

12. Baby Robbins describes the early states of idiopathic pulmonary fibrosis as "interstitial and intra-alveolar edema, interstitial infiltration by leukocytes, and type II pneumocyte proliferation"
- "Anthracosis is the small harmless accumulations seen in the lungs of urban dwellers and smokers" and the others are more obvious.

-Kalico --> D-day is tomorow! eek!
 
Can't remember if this was answered already, but dejavu is classically associated with temporal lobe epilepsy.
 
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