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Old 03-09-2012
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Wink Goljan + FA marathon.

I am doing goljan audio and slides along with FA 2012.

In this thread I will be posting any mismatches between these 2 sources.
I will really appreciate your help.

Goljan:

Red vs. Pale infarct
G. says that organs that have good consistency develop pale infarcts: Heart, Kidney, Spleen and Liver.

FA'12 says Liver has Red infarct, due to dual blood supply.
What to believe? 2 blood supply sounds more logic to cause red infarct.
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Old 03-09-2012
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I remember in uworld -> red infarct -> same explanation as FA 2012.

I tried looking for the question and explanation again in uworld, but I can't find it. I'll put it in this thread if I come across it again in my notes.
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Old 03-09-2012
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Default I have the same doubt

The Golj audio is said to be dated although most principles of Pathology remain forever true...

So, I continue to the first post: the risk of developing atherosclerosis is not high level of LDL but low level of HDL, for that matter women are protected for longer time than men... I have done many Qs ( but can't find them now),of which ans is high level of LDL... This pretty HY topic makes me worried.
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The questions in NBMEs usually come with a gross specimen picture! You can easily identify the type of infarct. The questions dont ask whether its a pale or red infarct. They simply write INFARCT in the options. Secondly, the organs with the dual blood supply have Red infarcts. Sometimes, Pale infarcts become red after Reperfusion! So, I think it depends a lot on the Question stem.
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Quote:
Originally Posted by patho2012 View Post
The Golj audio is said to be dated although most principles of Pathology remain forever true...

So, I continue to the first post: the risk of developing atherosclerosis is not high level of LDL but low level of HDL, for that matter women are protected for longer time than men... I have done many Qs ( but can't find them now),of which ans is high level of LDL... This pretty HY topic makes me worried.
well high HDL protects you from Atherosclerosis, but that doesn't mean that you can't have atherosclerosis.

Even if you have normal or high HDL but you're LDL is really really high then you will still get atherosclerosis.


There's 2 things that you have to be weary of here:

1. In most people, LDL is within normal range or marginally raised. Normally they are protected by their normal range of HDL. But if for whatever reason the HDL drops then even though they are in the normal range of LDL they will still develop atherosclerosis. This is what I believe Goljan was referring to. This represents the majority of the population, where HDL is the most important factor.

2. Now we look at the definite pathogenic state and this is what we are tested on in Step 1. When you have highly elevated LDL you will definitely develop atherosclerosis...its a no brainer. It's the concept that they want to test.


When listening to Goljan he spoke from a clinical perspective. At the time there were a few things I picked up that you will see as a practitioner. But on step 1 they are testing important basic concepts and theories. They ask questions on definite pathogenic states...things we should know for testing and less for real life medicine.
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In uworld there was a question with a lung that undergone hemorrhagic infarct from pulmonary emboli due to IVDA at the tricuspid.
why hemorrhagic? becuase it has dual blood supply
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Quote:
Originally Posted by haga View Post
well high HDL protects you from Atherosclerosis, but that doesn't mean that you can't have atherosclerosis.

Even if you have normal or high HDL but you're LDL is really really high then you will still get atherosclerosis.


There's 2 things that you have to be weary of here:

1. In most people, LDL is within normal range or marginally raised. Normally they are protected by their normal range of HDL. But if for whatever reason the HDL drops then even though they are in the normal range of LDL they will still develop atherosclerosis. This is what I believe Goljan was referring to. This represents the majority of the population, where HDL is the most important factor.

2. Now we look at the definite pathogenic state and this is what we are tested on in Step 1. When you have highly elevated LDL you will definitely develop atherosclerosis...its a no brainer. It's the concept that they want to test.


When listening to Goljan he spoke from a clinical perspective. At the time there were a few things I picked up that you will see as a practitioner. But on step 1 they are testing important basic concepts and theories. They ask questions on definite pathogenic states...things we should know for testing and less for real life medicine.
Read the Risk of Heart diseases recommended by NYHA, NIH or whatever... Read more about the Framinghan Heart Study, or simply wiki.
http://en.wikipedia.org/wiki/High-density_lipoprotein

The board knows your "no brainer " common sense and feast on that.
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Goljan:

In hypopituitarism, due to decreased ACTH stimulation, Fasciculata and Reticularis get atrofied, but Glomerulosa is just fine, because it is not stimulated by ACTH.


FA'12:

Cholesterol is a substrate for all 3 layers G F and R, ACTH stimulates desmolase to convert Cholesterol to Pregnenolone for further synthesis of the adrenal hormones.
Angiotensin II doest though convert corticosterone to aldosterone.

- based on fa it looks like all 3 zones will undergo athrophy with lack of ACTH stimulation
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Goljan:

Post translational modification of collagen (talking about defective lysine and proline hydroxilation, requiring vitamin C) happens in Golgi


FA'12:

Synthesis, hydroxilation and glycosilation - all in Endoplasmic Reticulum.
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Old 03-11-2012
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There can be two types of infarcts ( pale and red ) in the heart and liver and brain. Lungs and intestines are well known for red infarcts. Heart and kidneys and spleen are known for pale infarcts.

(Since the exam Qs are made based on Robbins, so it would be safer to go with Goljan. FA is too general to be precise).

Robbins p101:
Red infarcts occur with (1) venous occlusion for example ovarian torsion (2) in loose tissue that allow blood to collect in the infarcted zone (3)tissues with dual circulations;lungs and intestine (4)in tissues previously congested (5)reperfusion, ie when pts with MI are treated immediately, the previously necrotic tissue forms a red infarct. Otherwise a pale infarct is formed with congested and hyperemic border because blood reperfused the ischemic surrounding tissue.

White infarcts: occur (1)with arterial occlusion->hence they become pale and sharply defined with time (2) solid tissue that limits the amount of hemorrhage that seeps into the ischemic area. (3) in end-arterial organs: kidney, spleen.

Mechanisms and differentials are way to go.

Thanks,

Last edited by patho2012; 03-11-2012 at 04:41 PM. Reason: typos
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Old 03-12-2012
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Quote:
Originally Posted by DocSikorski View Post
Goljan:

Post translational modification of collagen (talking about defective lysine and proline hydroxilation, requiring vitamin C) happens in Golgi


FA'12:

Synthesis, hydroxilation and glycosilation - all in Endoplasmic Reticulum.
FA is correct.
Collagen article on Wiki:
Alpha Peptide to Procollagen in the ER:
...
From here the hydroxylated and glycosylated propeptide twists towards the left very tightly and then three propeptides will form a triple helix. It is important to remember that this molecule, now known as procollagen (not propeptide) is composed of a twisted portion (center) and two loose ends on either end. At this point the procollagen is packaged into a transfer vesicle destined for the golgi apparatus.
Golgi Apparatus Modification: In the golgi apparatus, the procollagen goes through one last post-translational modification before being secreted out of the cell. In this step oligosaccharides (not monosaccharides like in step 3) are added, and then the alpha peptide is packaged into a secretory vesicle destined for the extracellular space.

Thx.
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Old 03-13-2012
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FA'12:

decrease in delivery of NA to the juxtamedullary apparatus of the kidney => Renin release.

Goljan:

Increase of the plasma volume => decrease in renin release (low renin hypertension in blacks)

So what does cause the release of renin? (except for sympathetic stimulation) Is it low Na delivery or low plasma volume?
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Old 03-13-2012
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Quote:
Originally Posted by DocSikorski View Post
FA'12:

decrease in delivery of NA to the juxtamedullary apparatus of the kidney => Renin release.

Goljan:

Increase of the plasma volume => decrease in renin release (low renin hypertension in blacks)

So what does cause the release of renin? (except for sympathetic stimulation) Is it low Na delivery or low plasma volume?
Low NACL volume to be precise, the juxtaglomerular cells respond to low Na that happens to come most of the time with low volume state (not always tho); also in pseudohyponatremia renin release will be triggered in order to retain more salt and bring the osmotic level to equilibrium (or so i think...)
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mmmyeah... I wish I'd be doing Goljan seriously from the day one.
I used to go runnning with goljan playing in my headphones, but it takes more than that.
He is great.

Goljan:

Doin a digital examination does not increase PSA! Cuz its not an enzyme...
Its just a part of the structure within the cell.

I clearly remember my young surgery teacher who said the opposite.
Thanks Dr.G!
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Ok, now important part.
How old are these audio lectures?

Wikipedia says goljan was born in 1943.
In one of the audio files he just said that he was 58...
Are these lectures 10 years old??
uhm...
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Quote:
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Ok, now important part.
How old are these audio lectures?

Wikipedia says goljan was born in 1943.
In one of the audio files he just said that he was 58...
Are these lectures 10 years old??
uhm...
yes from 2002
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Quote:
Originally Posted by XpaezX View Post
Low NACL volume to be precise, the juxtaglomerular cells respond to low Na that happens to come most of the time with low volume state (not always tho); also in pseudohyponatremia renin release will be triggered in order to retain more salt and bring the osmotic level to equilibrium (or so i think...)
juxta respond to coc or amount of Na?
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Goljan:

gold standard of lab measuring for MI - CK-MB.
disappears after 3 days. (if reappears - denotes reinfarction)
...not Troponin. Troponin stays for 7 days, though its earlier than CK-MB.


UW:

Best test is Troponin.
Not CK-MB cuz the second appears later.
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Goljan calls Roth's spot in the infective endovarditis as "Koplik spot of the eye" because it is red with a white center as the Koplik spots in measels.

He then states that lesions (Janeway or Oslers and Roth's spot are due to Type III hypersensitivity and not to embolus)

Fa had a picture of blue-white Koplik spots on a buccal mucosa in a pt with measels
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Goljan:

Foreign body final destination in the lung:

Standing - posterior basal segment of the right lower lobe

Laying down - superior segment of the right lower lobe

Laying on the right side - Middle lobe OR Posterior segment of the right upper lobe.

FA'12

only confirms standing and general laying.

==================================================

Goljan:
Most common site of thrombus formation is DVT. But it is becoming dangerous for embolisation to the lung when the thrombus reaches the femoral vein.

Fa'12 - 95% are from DVT.
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Old 03-14-2012
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so which one is the "original" goljan high yield notes?
i have 4 different ones:
46 pages
59 pages
100 pages
123 pages
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Old 03-14-2012
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Quote:
Originally Posted by kenlee View Post
so which one is the "original" goljan high yield notes?
i have 4 different ones:
46 pages
59 pages
100 pages
123 pages
none of these mentioned.
He has 200+ pages notes for general pathology
and 200+ pages for systemic pathology.
All these 100, 36 pages are just someone's custom re-edit of original notes.
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Old 03-14-2012
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none of these mentioned.
He has 200+ pages notes for general pathology
and 200+ pages for systemic pathology.
All these 100, 36 pages are just someone's custom re-edit of original notes.
Goljan HY notes are notes he made for Falcon review courses. They are much better than the book Pathophysiology for B&W that is overrated.
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Old 03-16-2012
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Arrow what can appear as nodule(s) in hands and feet...

-particle microemboli in IVDA (tricuspid emdocarditis) vs. vegetation microemboli (mitral valve endocarditis).
-cholesterol microemboli (warfarin) and atherosclerosis emboli.

Osler's vs. Janeway's:
-Janeway's is septic emboli,hence painless.
-Osler's is deposit of imm complex, causing local inflammation, hence is painful.
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