Confused

[viper]

---

Members do not see this ad.

Some questions:

Is polyarteritis nodosa associated with ANCA? Goljan and several other review books (BRS path, etc) say yes. First aid and robbins say NO. Which one???

Is a liver infarct pale or hemorrhagic? goljan says pale - reasoning is the consistency of tissue even with the double blood supply. First Aid says hemorrhagic as well as some other sources - which is it???


Thanks,

 

[HiddenTruth]

Some questions:

1. Is polyarteritis nodosa associated with ANCA? Goljan and several other review books (BRS path, etc) say yes. First aid and robbins say NO. Which one???

2. Is a liver infarct pale or hemorrhagic? goljan says pale - reasoning is the consistency of tissue even with the double blood supply. First Aid says hemorrhagic as well as some other sources - which is it???


Thanks,

1. brs and goljan are wrong. There is NO association of ANCA with PAN.
2. from what i know, liver infarcts are very rare to begin with (bc of the dbl blood supply). But, regardless, I have always thought pale. The only tissues with hemorrhagic infarcts that i know are lungs, testes, and oolon. did you check robbin's?

 

[viper]

1. brs and goljan are wrong. There is NO association of ANCA with PAN.
2. from what i know, liver infarcts are very rare to begin with (bc of the dbl blood supply). But, regardless, I have always thought pale. The only tissues with hemorrhagic infarcts that i know are lungs, testes, and oolon. did you check robbin's?

Thanks Hiddentruth - I am going with NO association with ANCA on that.

You are right liver infarcts are very rare. Others answer red - but I think they are confusing with "nutmeg liver" which I think of as congestion and not an infarct (am I right?). But I have found no definitive answer yet - Goljan says pale, First Aid says red. Robbins could be the deciding factor - but I couldn't find it in there (not saying it's not in there, but anyone know where?).

Thanks,

 

[adrenal_medulla]

Thanks Hiddentruth - I am going with NO association with ANCA on that.

You are right liver infarcts are very rare. Others answer red - but I think they are confusing with "nutmeg liver" which I think of as congestion and not an infarct (am I right?). But I have found no definitive answer yet - Goljan says pale, First Aid says red. Robbins could be the deciding factor - but I couldn't find it in there (not saying it's not in there, but anyone know where?).

Thanks,

Robbins says usually pale but sometimes hemorrhagic. You should find it around page 917. I looked it up on the Robbins website.

 

[adrenal_medulla]

I found this about ANCAs and PAN.

 

[Idiopathic]

Thanks Hiddentruth - I am going with NO association with ANCA on that.

Boo. Very wrong. You actually can see both, but P-ANCA is more common with polyarteritis nodosa. Keeping in mind that neither is diagnostic of the condition, either CAN be seen.

As far as a liver infarct, they are pale, but can sometimes be mottled ("infarct of Zahn")

 

[HiddenTruth]

Boo. Very wrong. You actually can see both, but P-ANCA is more common with polyarteritis nodosa. Keeping in mind that neither is diagnostic of the condition, either CAN be seen.

As far as a liver infarct, they are pale, but can sometimes be mottled ("infarct of Zahn")

Actually, I really don't think you do, despite the content in that link posted. It must be a new "finding" or something, because last years FA had it, and most of the sources show that there is an association (brs, goljan, etc.), but if you look in the latest robbins, there is no association of P-ANCA with PAN, and I don't believe that the latest FA has it shown either.

 

[Ruban]

I dunno, but if I miss a question on P-ANCAs in PAN I am gonna be pissed 😱

 

[HiddenTruth]

I dunno, but if I miss a question on P-ANCAs in PAN I am gonna be pissed 😱

read robbins

 

[Ruban]

read robbins

But Robbins (who says there is no P-ANCA) disagrees with all my other sources. Still, I am gonna stick w/ Robbins.

 

[mattie113]

i lost the link so you will either have to take my word on it or look for it yourself but the publisher of First Aid has a page of various corrections and errors in the 2005 edition - according to them it is supposed to say that there IS a relationship between PAN and P-ANCA.
and also they corrected the inside front cover page references (if you try to use the subject page references you will find that none of them are correct)

 

[caribsun]

Polyarteritis nodosa has a PANCA relationship...everything i have says it

and wegeners granulomatosa has what relationship? .... 🙂

 

[streetdoc]

my thoughts are this...
if it is a debated subject, i doubt you see a direct question on the topic...also (all my souces say there is P-anca) anything that has changed in the past year is probably too new to make it onto the step exam...then again, i may be thinking incorrectly but i'm not losing sleep over something like this.
streetdoc

 

[Idiopathic]

Actually, I really don't think you do, despite the content in that link posted. It must be a new "finding" or something, because last years FA had it, and most of the sources show that there is an association (brs, goljan, etc.), but if you look in the latest robbins, there is no association of P-ANCA with PAN, and I don't believe that the latest FA has it shown either.

If there is this much debate on the topic, then it wont be a question-breaker on step 1. However, you cannot rule out/in PAN based on a positive/negative p-ANCA. It is sometimes there, sometimes not...that is the simple fact.

 

[maverick_pkg]

If there is this much debate on the topic, then it wont be a question-breaker on step 1. However, you cannot rule out/in PAN based on a positive/negative p-ANCA. It is sometimes there, sometimes not...that is the simple fact.

p- anca is present in <20% of PAN cases - ref: Harrisons's principles of internal medicine

wegeners is associated with c-anca

 

[viper]

Alright I have another one for you guys (since the last one helped a lot - see positive reinforcement).


This has to do with Law of Laplace (P = 2HT/r).

I get how this has to do with ventricular hypertrophy --> increase height, increase pressure.
I get how this has to do with alveoli --> decrease r and collapsing pressure increase --> thus need surfactant
Also I have read that this has to do with aneurysms --> increasing diameter causes increasing wall stress and eventually an aneurysm will rupture. Can someone please explain this - I would think this would be equivalent to increasing r and thus pressure decreases (which is why it must of happened in the first place - as a compensation to the stress). So what am I missing.

have at it and thanks again,

 

[maverick_pkg]

Alright I have another one for you guys (since the last one helped a lot - see positive reinforcement).


This has to do with Law of Laplace (P = 2HT/r).

I get how this has to do with ventricular hypertrophy --> increase height, increase pressure.
I get how this has to do with alveoli --> decrease r and collapsing pressure increase --> thus need surfactant
Also I have read that this has to do with aneurysms --> increasing diameter causes increasing wall stress and eventually an aneurysm will rupture. Can someone please explain this - I would think this would be equivalent to increasing r and thus pressure decreases (which is why it must of happened in the first place - as a compensation to the stress). So what am I missing.

have at it and thanks again,

Laplace law: pressure = wall tension/radius (p=t/r)
ie pxr=t

thus as radius increases wall tension increases which causes radius to increases even more..... rupture

 

[streetdoc]

ahhh yet another goljan phrase. this is the first year i remember seeing soooo much about/from him on SDN. is this his break through year? or did i just miss his stuff the past years...?
also, i agree, this is helpful. you should check over the pimp thread.
streetdoc

 

[dynx]

Alright I have another one for you guys (since the last one helped a lot - see positive reinforcement).


This has to do with Law of Laplace (P = 2HT/r).

I get how this has to do with ventricular hypertrophy --> increase height, increase pressure.
I get how this has to do with alveoli --> decrease r and collapsing pressure increase --> thus need surfactant
Also I have read that this has to do with aneurysms --> increasing diameter causes increasing wall stress and eventually an aneurysm will rupture. Can someone please explain this - I would think this would be equivalent to increasing r and thus pressure decreases (which is why it must of happened in the first place - as a compensation to the stress). So what am I missing.

have at it and thanks again,

The problem you are having is you're putting the change in response to Radius on the pressure side of the equation. The pressure in an aneurysm is Arterial blood pressure, it doesn't change based upon the size of the aneurysm. So if the radius increases yet pressure stays the same what must increase? Tension...it must go up to make the right side of the equation match the left. More wall tension = more damage = rupture.

 

[viper]

Dynx - I like that explanation - THANKS


Although now another question comes to mind. In the heart - the p is pressure that can be generated from the wall (is this correct?) --> to compensate for increased afterload.
In the lung it is collapsing pressure - again I assume from the wall.
Then why in the aneurysm scenario the pressure now is blood pressure (assuming you mean the pressure coming from the heart and not the wall itself here - as the pressure exerted by wall would actually be decreased). My question is what is P? how do you figure out what it is? I would have said it's P from the wall and p slightly should have decreased here owing to dilatation of the wall.

Alternatively I was starting to think about it this way - though not sure if this is correct. Perhaps the radius and T are dependent variables - meaning a change in one necessarily has a change in the other (sort of similar to CO and TPR in BP - if that makes sense?) Is this assumption correct??

 

[dynx]

Dynx - I like that explanation - THANKS


Although now another question comes to mind. In the heart - the p is pressure that can be generated from the wall (is this correct?) --> to compensate for increased afterload.
In the lung it is collapsing pressure - again I assume from the wall.
Then why in the aneurysm scenario the pressure now is blood pressure (assuming you mean the pressure coming from the heart and not the wall itself here - as the pressure exerted by wall would actually be decreased). My question is what is P? how do you figure out what it is? I would have said it's P from the wall and p slightly should have decreased here owing to dilatation of the wall.

Alternatively I was starting to think about it this way - though not sure if this is correct. Perhaps the radius and T are dependent variables - meaning a change in one necessarily has a change in the other (sort of similar to CO and TPR in BP - if that makes sense?) Is this assumption correct??

The pressure IN the vessel and the "collapsing pressure" as you state it are one in the same if the system is in stasis. In other words, when the aneurysm expands the pressure exerted by its wall does NOT decrease. It would decrease if tension didn't rise to adjust for the increased radius.

In the lungs however you have an open system for flow, the collapsing pressure of small alveoli is greater than the avg. interalveolar pressure on the lung and you therefor have collapse with air flow to larger alveoli.

Your dependent variable thought is correct. In the lungs you want to have equal pressure across the alveoli, so if some of the alveoli are smaller you need to decrease the tension in them too.

In the heart its different depending upon the problem.