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  #1  
Old 02-22-2012
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Default Heart condition in the immigrant question.

10-yr. old immigrant from Eastern Europe is brought to clinic with exertional dyspnea and easy fatigability. To his parents, he was diagnosed with a congenital heart disease (type unknown) in infancy, but they refused surgical correction. On the examination - toe cyanosis and clubbing, but no finger abnormalities. The patient suffers from:

A. Primum-type ASD
B. Secundum-type ASD
C. VSD
D. PDA
E. Coarctation of the aorta
F. Tetralogy of Fallot


Taken from the UW. I think this question is very unfair. Lets discuss after you come up with an answer
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Old 02-22-2012
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The answer is Coarctation of Aorta Preductal coarctation type . This is uw QUESTION i had got it wrong the first time.I just figured out in a way that For cyanosis to occur there should be deoxygenated blood supply in that organ,in this situation it could only happen if there is preductal coarctation which will ultimately lead to increase in PULMONARY ARTERY pressure leading to deoxygenated blood in aorta so deoxygenated blood supply in lower limb causing cyanosis.

I still find this question very confusing
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Old 02-22-2012
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its E and its a very rare case, i had to look it up in wikipedia to know it :\
Its very tricky
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Old 02-22-2012
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It's D --> PDA

There is a huge Coarctation of the Aorta (COA) picture in the explanation but the answer is PDA. (The COA pic made everything confusing. I also actually initially thought COA was the right answer because of the lay-out and huge pic.)

I wouldn't have guessed that the boy developed pulmonary HPN, leading to a R -> L shunt, causing the differential cyanosis.

A very WTF question to me. LOL!
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Old 02-22-2012
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Quote:
Originally Posted by d_wiqed View Post
It's D --> PDA

There is a huge Coarctation of the Aorta picture in the explanation but the answer is PDA.

I wouldn't have guessed that the boy developed pulmonary HPN, leading to a R -> L shunt, causing the differential cyanosis.

A very WTF question to me. LOL!

yes felt the same .... Coarctation does not cause cyanosis as renal compensation by renin cause HT in UL and normal blood volume in LL ... PDA if not corrected over long time cause differential cyanosis ......
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Old 02-22-2012
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Yes its wtf :\
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Old 02-22-2012
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Yes I red explanation once again and it made it clear to me.

I thought COA too first.

Very tricky in my opinion. Especially if you memorize ASD VSD and PDA to be noncyanotic...


btw it is question #394877 in UW
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Last edited by DocSikorski; 02-22-2012 at 10:53 AM.
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Old 02-23-2012
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Default PDA with Eisenmengerisation.

Even though it seems to be, it doesn't have to be that tough. As far as I've known, we have to note the points that matter in the question.

In this case, they're hinting at "Differential cyanosis". I can't think of any other thing causing this typical condition than a latent PDA which has Eisenmengarised.
Mechanism - In this condition, deoxygenated blood from the pulmonary artery is shunted into the aorta, "distal" to the left subclavian artery. Hence, the blood supply to the upper limb is unaffected, whereas the lower limb receives the shunted deoxygenated blood - causing differential cyanosis and differential clubbing.
So if you get any question hinting at cyanosis/clubbing ONLY in the toes; don't scratch your heads, you already know the answer.

Similarly the buzzword for Coarctation of Aorta is radiofemoral delay...

(PS - Differential Clubbing was one of the short questions in our Pediatrics exam, Heh!)
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