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Zuhal

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68 yo male patient presents to your clinic with postprandial pain. X-ray below, whats the dx?

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Decreased cross sectional area due to arterioles being non-compliant?

I'm horrible with vasculitis/heart so this is a complete shot in the dark

Cardio isn't my fav either but this has noting to do with compliance. Think resistance.
 
AVM associated with Sturge weber -> increased preload. Not sure what exactly causes reduced after load though.

Right on!
Sturge Weber--> leptomeningeal angiomatosis--> AVM--> Increase in blood returning to the heart (shunt)= increase preload. The AVM= bypassing arterioles (major points of resistance)= decrease in afterload. All of which increase stroke volume and could potentially lead to a high output heart failure
 
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AVM associated with Sturge weber -> increased preload. Not sure what exactly causes reduced after load though.

Ha!! yeah, AVMs are like AV fistulas in that they cause high output heart failures. The increased pre-load will causing increased CO (through increased ventricular stretch/contraction).. but I also don't see the decreased preload.

Edit: LOL... just was Zuhal's post above, I get it now!
 
Which type of drug long term can cause this.

Don't know what I'm looking at here... the speckles in the mediastinal area, or the fact that the lung field is really black.

Higher yield lung pathology that's drug related is typically pul fibrosis... in which case, it could be Bleomycin, Bulsulfan, Amiodarone.... or long term methotrexate.

Probably wrong.
 
Don't know what I'm looking at here... the speckles in the mediastinal area, or the fact that the lung field is really black.

Higher yield lung pathology that's drug related is typically pul fibrosis... in which case, it could be Bleomycin, Bulsulfan, Amiodarone.... or long term methotrexate.

Probably wrong.

I was thinking the same thing but it doesn't look like fibrosis. maybe gas? there's something wrong with the diaphragm
 
GJ. mechanism please?

perforated gastric ulcer is all i can tell you unfortunately lol. we had a question just like this on our exam

by the way, i just found this thread today. thank you so much for this, it is soo helpful.

i will be on the lookout for images I can add :)
 
I was thinking the same thing but it doesn't look like fibrosis. maybe gas? there's something wrong with the diaphragm

oh i see it now...

sharklasers
perforated gastric ulcer is all i can tell you unfortunately lol. we had a question just like this on our exam

by the way, i just found this thread today. thank you so much for this, it is soo helpful.

i will be on the lookout for images I can add

that makes a lot of sense now. thanks for the explanation
 
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Yup, the diaphragm is a good place to focus.

My xray/CT/MRI interpreting skills are not that good (and neither is my anatomy haha) but if you perforate the diaphragm in a surgical procedure or maybe a stab wound, wouldn't u get a similar presentation? but you're looking for a drug right?
 
My xray/CT/MRI interpreting skills are not that good (and neither is my anatomy haha) but if you perforate the diaphragm in a surgical procedure or maybe a stab wound, wouldn't u get a similar presentation? but you're looking for a drug right?

Sharklasers already got NSAID though... and the mechanism he provided seemed to make sense to me.
 
linitisplastica.jpg


this dude's stomach is rock hard...what pathology, and what would you see on histology to confirm said pathology?
 
Oh? sorry i didn't see that. how does it do that?


There's air in the stomach (bloaty feeling we often get after crazy nachos), generated from gastric bacteria... and I was thinking since NSAID caused the perforation, the only place the air would go after reching the intra-peritoneal space is up..right up underneath the diaghram.
 
There's air in the stomach (bloaty feeling we often get after crazy nachos), generated from gastric bacteria... and I was thinking since NSAID caused the perforation, the only place the air would go after reching the intra-peritoneal space is up..right up underneath the diaghram.

WOW good reasoning! and good question too :thumbup:
 
There's air in the stomach (bloaty feeling we often get after crazy nachos), generated from gastric bacteria... and I was thinking since NSAID caused the perforation, the only place the air would go after reching the intra-peritoneal space is up..right up underneath the diaghram.

Yup thats correct, And FYI the finding is called pneumoperitoneum.
 
There's air in the stomach (bloaty feeling we often get after crazy nachos), generated from gastric bacteria... and I was thinking since NSAID caused the perforation, the only place the air would go after reching the intra-peritoneal space is up..right up underneath the diaghram.

Yessirrr... what's the pathology or name of the disease?

Linitis plastica
 
You see the slow drop after the S wave, like a steady gradual drop, and a step rise? That's supposed to be a sign of LVH (HTN for ex.). But idk if that's what this is. It's not seen in every complex. That's all I can see.
 
I see some ST depression and T wave inversion - that points to ischemia though. Stable angina, or less than 75% occlusion of the coronary artery?

Digoxin toxicity? That's basically always my guess when I have no idea what the ECG is showing LOL

Digoxin tox was my guess because of the scoops. They aren't quite "scoops" though (hint #2)

Also there was no mention of ischemia in the answer stem, I don't think it can be ischemia if it is paraxysomal as in this lead (only recordings 2,3,4 show the "depression")
 
Heart block? 1st degree?

That would be elongated PR, this is a short PR.

You see the slow drop after the S wave, like a steady gradual drop, and a step rise? That's supposed to be a sign of LVH (HTN for ex.). But idk if that's what this is. It's not seen in every complex. That's all I can see.

Not LVH, though they share a similarity in that the current takes a longer time to depolarize the ventricles. Hence the widened QRS on 2,3,4
 
Hopefully I don't **** this question up, going to try to have a bit of a stem attached

40 y/o caucasian female with no significant PMHx presents to PCP w/exertional dyspnea. She returned a month ago from a mission trip to south asia. She mentions to you that the trip was uneventful and that she enjoyed building huts in the dirt and eating seafood with the locals, though she had a few days of stomach cramping and loss of appetite. CBC reveals

HBG - 9.8
HCT - 30
MCV - 87
PLT - 200k
WBC - 7k

The PBS is attached.

Over the next month, if you decide to watch her condition and see what happens, the most likely development will be

A) Peripheral neuropathy
B) Ringed sideroblasts
C) Elevated free erythrocyte protoporphyrin
D) Dilated cardiomyopathy

I think I made there be one most likely answer... But if I didn't I apologize :x
 

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WPW? although I don't see a clear delta wave...

Correct, I had a hard time with the delta waves as well yet it claims that this is classic.

The explanation:


The EKG is classic for WPW syndrome. WPW syndrome is caused by pre-excitation of the ventricles due to an accessory pathway (the bundle of Kent). Patients are often asymptomatic or may have nonspecific symptoms. On EKG, look for the delta wave (slurred upstroke in the QRS complex), short PR interval, and widened QRS as seen in the exhibit.
 
Hopefully I don't **** this question up, going to try to have a bit of a stem attached

40 y/o caucasian female with no significant PMHx presents to PCP w/exertional dyspnea. She returned a month ago from a mission trip to south asia. She mentions to you that the trip was uneventful and that she enjoyed building huts in the dirt and eating seafood with the locals, though she had a few days of stomach cramping and loss of appetite. CBC reveals

HBG - 9.8
HCT - 30
MCV - 87
PLT - 200k
WBC - 7k

The PBS is attached.

Over the next month, if you decide to watch her condition and see what happens, the most likely development will be

A) Peripheral neuropathy
B) Ringed sideroblasts
C) Elevated free erythrocyte protoporphyrin
D) Dilated cardiomyopathy

I think I made there be one most likely answer... But if I didn't I apologize :x

I'm going with "A" but I literally see nothing wrong with that image outside the possibility of a slight microcytosis but with the MCV I doubt that. The question stem points me towards
D.Latum.

Edit: On second thought I don't really like A as it would take longer than a month to go through the livers B12 storage
 
Correct, I had a hard time with the delta waves as well yet it claims that this is classic.

The explanation:


The EKG is classic for WPW syndrome. WPW syndrome is caused by pre-excitation of the ventricles due to an accessory pathway (the bundle of Kent). Patients are often asymptomatic or may have nonspecific symptoms. On EKG, look for the delta wave (slurred upstroke in the QRS complex), short PR interval, and widened QRS as seen in the exhibit.

Nice. does anyone remember the DOC? what drugs are c/i?
 
Correct, I had a hard time with the delta waves as well yet it claims that this is classic.

The explanation:


The EKG is classic for WPW syndrome. WPW syndrome is caused by pre-excitation of the ventricles due to an accessory pathway (the bundle of Kent). Patients are often asymptomatic or may have nonspecific symptoms. On EKG, look for the delta wave (slurred upstroke in the QRS complex), short PR interval, and widened QRS as seen in the exhibit.

that's crazy... it doesn't show a classic pic of WPW... on second take I can slightly see it on the last QRS spike

wpw_sy1.gif
 
that's crazy... it doesn't show a classic pic of WPW... on second take I can slightly see it on the last QRS spike

wpw_sy1.gif

To be fair I think the 3rd depolarization looks a lot nicer than your V2,V3.
But I'd agree your I,V5, V6 is what I'd call classic
 
To be fair I think the 3rd depolarization looks a lot nicer than your V2,V3.
But I'd agree your I,V5, V6 is what I'd call classic

true that... i really do hope they give us something easier to read on the step 1 exam though... none of the realistic BS...I want fake stuff.. that's easier to get, lol
 
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