Questions on Concepts with Conflicting Information

[SKaminski]

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Hey everyone!

I've been study for Step 1, and creating flashcards from lecture notes/FA/Pathoma/SketchyMedical. Sometimes, however, these sources conflict in information, and other times I am still confused by concepts.

1) Is poliovirus spread only fecal-orally, or through respiratory droplets as well?

2) Emphysema question from anki: Which COPD involves enlarged alveoli that are separated by thin septa (on microscopy)? Why is the answer to this question Emphysema and not Bronchiectasis? I understand that emphysema destroys collagen, but would this really cause thin septa?

3) Is their a difference between a pleural effusion and a hydrothorax, or are they the same thing?

4) Any good tips for understanding S3/S4? I just can't wrap my head around understanding what creates what sound, and more importantly why.

4) Adequate levels of surfactant: Are they reached during the 34th week or the 35th week?

5) Is a P-ANCA seen in Ulcerative Colitis AND in Crohns Disease, or ONLY Ulcerative Colitis?

6) Is Chromogranin A expressed in onlny Carcinoid Tumors, or in both Carinoid Tumors and small cell lung carcinomas?? (Both are derived from neuro-endocrine cells)

7) What is meant by "Clara Cells Act as reserve cells"? It is the type 2 pneumocytes that are the stem cells .

I have many more questions, but i'll leave it at these 7 for now.

 

[StilgarMD]

1) I've only ever seen it as fecal-oral, confirmed w/ Wiki

2) Emphysema is a disease of excessive structural damage from too much Protease/Metalloprotease/etc activity or insufficient Anti-Protease/TIMP activity. These enzymes are regularly secreted and in excess, they will chew apart the septa. my understanding of Bronchiectasis is frequent infections and subsequent scarring taking place in the larger airways, which will eventually obstruct the path for air to leave, but the alveoli should be intact.

3) Pleural effusion is any fluid in the pleural cavity. Hydrothorax is a water pleural effusion, Hemothorax is a blood one, etc.

4) S3 is swishing sound (at least how I think of it) and can be caused by overzealous atrial activity or by a normal atria pushing into a Fluid overloaded ventricle. S4 is the sound the atria makes, and it makes it because its pushing against great force, either due to a fluid overloaded Ventricle OR a restrictive/hypertrophed ventricle. S3 = Fluid, S4 = Atria. Maybe wrong, but its how I think of it.

5) Latest edition of Golijan's RR says p-ANCA is UC specific, "iritis (CD > UC), primary sclerosing cholangitis (UC > CD)" pg 457.

6) I've read that SCLC has granules, and would be inclined to believe that Chromogranin A would be present in both (Along w/ Neuro-Enolase and Synaptophysin, maybe S100)

7) They have similar to function to Type II Pneumocytes, but they make Minor surfactant components. Not sure about the Reserve thing, though they do divide.

 

[worldbeater]

4) S3 is swishing sound (at least how I think of it) and can be caused by overzealous atrial activity or by a normal atria pushing into a Fluid overloaded ventricle. S4 is the sound the atria makes, and it makes it because its pushing against great force, either due to a fluid overloaded Ventricle OR a restrictive/hypertrophed ventricle. S3 = Fluid, S4 = Atria. Maybe wrong, but its how I think of it.

S3 -> fluid overload in a dilated heart, which is correct
S4 -> fluid hitting a stiff ventricle, atria isn't involved in making the noise. 90% of the fluid is falling from the atria to the ventricle due to gravity.

 

[StilgarMD]

S3 -> fluid overload in a dilated heart, which is correct
S4 -> fluid hitting a stiff ventricle, atria isn't involved in making the noise. 90% of the fluid is falling from the atria to the ventricle due to gravity.

S4 takes place at the very end of diastole because it represents the final push of fluid from the Atria into the ventricles. Atrial contraction doesn't contribute much to the movement of fluid at rest in a normal heart, but in this fluid overloaded state it likely does. The passive filling of the ventricles is driven by the drop in pressure the dilating cavity pulling fluid out of the atria. I believe the atria still contract, and the noise is caused by that contraction against a restrictive (either due fluid overloading or wall thickening) Ventricle. The ventricles may be normally compliant yet still produce an S4 in the fluid overloaded state produced by regurgitant valves. This is both what Wikipedia and GRR state.

 

[Transposony]

90% of the fluid is falling from the atria to the ventricle due to gravity.

 

[SKaminski]

Thank you @StilgarMD and @worldbeater , ya'll are great. Thank you 🙂