USMLE images
Started by Zuhal
Procanimide, I'd imagine contraindications are if you develop drug induced lupus or if you suffer from Long QT syndrome on top of WPW
haha yea, misread that. But the MCV isnt <80 and its been a month since she returned.
This is pointing towards some sort of lead poisoning from lead painting huts or lead based bowls she ate with...she complain's of stomach ache...but then options A-C could occur with lead poisoning; which would you see in 1month? I'll go with (B) Ring Sideroblast... cos it takes about 1month for RBCs to mature
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Well the minute I saw your answer I thought..."Hookworm". Which would give you your answer.
FWIW, currently the picture doesn't show hypochromia, though it may show microcytosis but you really need a micrometer to call that as it would be really slight.
I'll go ahead and give my answer, since the question may be iffy. Question stems are harder to make both difficult and unambiguous than I would have thought!
So the answer I had in mind was C. Exposure of skin to dirt -> ancylostoma infxn -> iron deficiency anemia, which classically presents with a N/N phase before progressing to hypo/micro. Elevated free erythrocyte protoporphyrin is a pretty specific finding to IDA
The PBS is definitely normochromic (and possibly microcytic, but I gave the MCV to correct for that possibility - had a hard time finding a perfect image). The PMN in the image is not hypersegmented (requires 6+ lobes).
A - The 1st lab finding in megaloblastic anemia is classically hypersegmented PMN's. In symptomatic anemia with decreased HGB/HCT, you'd be past the point of having hypersegmented PMN's. Seafood was a lead to d. latum, but the CBC/PBS doesn't support that, and neither does the time frame to development of symptoms, unless she was already borderline B12 deficient (folate deficiency would more likely happen in that time frame)
B - I don't think lead poisoning has much/any of an N/N phase prior to other hematological changes. Basophilic stippling should be apparent on PBS if that were the case as well
D - Wrong location to contract chagas, which to my knowledge isn't associated w/the development of anemia either
If you think another answer is equally valid, please put forward the argument for my own edification purposes!
So the answer I had in mind was C. Exposure of skin to dirt -> ancylostoma infxn -> iron deficiency anemia, which classically presents with a N/N phase before progressing to hypo/micro. Elevated free erythrocyte protoporphyrin is a pretty specific finding to IDA
The PBS is definitely normochromic (and possibly microcytic, but I gave the MCV to correct for that possibility - had a hard time finding a perfect image). The PMN in the image is not hypersegmented (requires 6+ lobes).
A - The 1st lab finding in megaloblastic anemia is classically hypersegmented PMN's. In symptomatic anemia with decreased HGB/HCT, you'd be past the point of having hypersegmented PMN's. Seafood was a lead to d. latum, but the CBC/PBS doesn't support that, and neither does the time frame to development of symptoms, unless she was already borderline B12 deficient (folate deficiency would more likely happen in that time frame)
B - I don't think lead poisoning has much/any of an N/N phase prior to other hematological changes. Basophilic stippling should be apparent on PBS if that were the case as well
D - Wrong location to contract chagas, which to my knowledge isn't associated w/the development of anemia either
If you think another answer is equally valid, please put forward the argument for my own edification purposes!
One thing I definitely should have put in there is how long she was in Asia, wasn't thinking there
IDA time course is pretty variable based on prior nutrition status - I don't know of a rule of thumb for timing it. Dx mostly based on labs
It's been a month since she's been back
IDA time course is pretty variable based on prior nutrition status - I don't know of a rule of thumb for timing it. Dx mostly based on labs
It's been a month since she's been back
Nah, it was a good question and I was able to put it together after iwantto put his original thought up...
If you would have asked what would you expect to see in "6 months" then it really could have been either A or C but as it stands it was a well thought out question, give yourself credit.
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Are you thinking of EBV with Atypical lympocytes?
To my knowledge there is no disease with neutrophils doing such a thing, I believe in that picture it is just due to slide prep
Dx and what this cxr is commonly referred to?
Going to start out cold with just cxr and will add info, not sure how good people are with xrays
Is there hemidiaphragm paralysis? That's a shot in the dark
Nah good guess though.
Time for clinical vignette: Baby boy shows cyanosis on his APGAR that doesn't improve after 5 minutes.
NRDS? I feel like I should be seeing some right heart that I'm not seeing though, like there's deviation to the left. I'll give up and let other people guess after this one. Haven't looked at many films since 1st year
It's the heart we're looking at.
This cxr has a "name" which gives it a definitive diagnosis
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Radiologists and pathologists name everything after food. None of these things look like food
So I looked it up: procainmide is the DOC. CCB and digoxin are contraindicated.
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I know chagas causes dialated cardiomyopathy but I've never seen it associated with a fib? care to elaborate 🙂
Either way, this is not an a-fib recording
Dialated cardiomyopathy produces an S3 hrt sound=venticular gallop; doesn't really affect the atria that much
I wasn't seeing it as the a wave being high, I was seeing a low c wave...as in the ventricles weren't applying enough force to push the cuspids back up.
Additionally you're more likely to hear the S3 through a restrictive myopathy or a hypertrophic cardiomyopathy
Any hints on this one? I don't even know where to start with this.
Are you sure? S3 is heard in a dialated ventricle (FA2012 pg. 283). S4 is heard in a hypertrophied heart. I don't know about restricted cardiomyopathy, you could very well be right.
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Of course, this is a 25 y/o IVDA
this one's really tricky, it just shows a huge y descent (i.e. atrial emptying)...
... with the new hint - staph aureus would be a causative agent... so a dilated atria would cause the huge y-descent, so would that be mitral/tricuspid stenosis?
Constrictive pericarditis. That rapid y-descent has me thinking a restrictive pericardium is forcing blood from the RA to the RV at a high rate.
I agree this one is kind of tricky. Look at the v wave, it shouldn't be as prominent as it is in this figure. V wave corresponds to ventricular contraction when the tricuspid valve is closed. The atria is filling during this time. If we have Triscupid regurgitation as would be the case in an IVDA infected with staph aureus, the blood backs up into the atria and the V wave becomes more prominent.
I remember this from a question!! Constrictive pericarditis causes a rapid y-descent but I don't know how the 'a' and 'v' waves would look like? do you think they would be equal in 'prominence'?
This is what Wiki has to say about JVP and constrictive pericarditis:
Kussmaul's sign (raised JVP on inspiration)
increased JVP (almost universal), rapid y descent (prominent diastolic collapse of JVP)
As for the prominence I have no clue, hmmmm
You're both right, I always mix these two up. Figured by now they'd be down pat enough for me to speak with some authority...f'n cardio.
Edit: Well now I find this:
"In
constrictive pericarditis,
the S3 is called a pericardial knock, as it oc
curs slightly earlier and is of higher pitch.
The fourth heart sound is usually
seen in context with significant
aortic stenosis,
Dialted and Hypertrophic
Cardiomyophaty (HCM), systemic hypertension
and in
coronary artery diseases."
Guess I'll move this over to the difficult concepts thread
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