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 +0  (nbme22#24)

is this question asking what we physically pass through or by?

impostersyndromel1000  no, basically the question is testing if you know the branches of the abdominal aorta and which is closest to the renal (in this case, inferior to the renal arteries)
impostersyndromel1000  what you are passing by would better answer your question actually

 +0  (nbme23#41)

I thought ablation of the av node was a tx for a fib not heart block?


 +0  (nbme20#21)

according to uworld hypersensitivity pneumonitis is due to dust and that was also an option....

amarousis  so it's definitely dust but the specific type of dust was the most important in this question. the fact that they mentioned the birds is important. the dusty books would cause it but the bird dust is more important -.-
charcot_bouchard  Hypersensitivity Pneumonitis - Organic dust (like moldy hay) Pneumocniosis - Inorganic dust none help here though because both will present with same restrictive lung disease picture. i think since dust in library arent neither organic or inorganic and also u dont see many librarians with lung disease but bird ownership is specifically mentioned as cause of HP disease.

 +0  (nbme20#21)

how do we know parakeets cause hypersensitivy pneumonitis

smc213  FA18 p.657 bird exposure--> HSN pneumonitis (restrictive lung disease) and FA18 p.214 granulomatous diseases: foreign material-->HSN pneumonitis. I had to make sense of it since I didn't know it was HSN pneumonitis at first.




Subcomments ...

His tidal volume was 500 mL. End-expiratory was +5 cm and end-inspiratory was +25. We were supposed to use the difference in airway pressure, and not the end-inspiratory pleural pressure (+20).

Compliance = ΔV/ΔP = 500 / 20 = 25 mL/cm H2O

some-zheimers  Great explanation. In general, also a great idea to pay attention to the units. I studied Physics in undergrad and have got one or two questions based purely on following the units, when the formula slips. +2  
endochondral1  is that equation in FA? +  
redvelvet  yes @endochondral1, at page 651 in 2019FA +  


submitted by bubbles(31),

Basement membrane integrity is the determinant of full lung recovery following pulmonary insult.

Summary:

(1) loss of basement membrane integrity is critical in determining the “point of no return,” and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis;

(2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis;

(3) transforming growth factor-β is necessary, but not entirely sufficient, to promote permanent fibrosis;

(4) persistent injury/antigen/irritant is critical for the propagation of fibrosis;

(5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an “antigen(s),” chronic inflammation, and fibrosis; and

(6) unique cells are critical cellular players in the regulation of fibrosis.

citation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/

kernicterusthefrog  Lovely +  
endochondral1  any FA or pathoma or uworld correlation? +  
endochondral1  or was this a random? +  


submitted by bubbles(31),

Basement membrane integrity is the determinant of full lung recovery following pulmonary insult.

Summary:

(1) loss of basement membrane integrity is critical in determining the “point of no return,” and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis;

(2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis;

(3) transforming growth factor-β is necessary, but not entirely sufficient, to promote permanent fibrosis;

(4) persistent injury/antigen/irritant is critical for the propagation of fibrosis;

(5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an “antigen(s),” chronic inflammation, and fibrosis; and

(6) unique cells are critical cellular players in the regulation of fibrosis.

citation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/

kernicterusthefrog  Lovely +  
endochondral1  any FA or pathoma or uworld correlation? +  
endochondral1  or was this a random? +  


submitted by drdoom(212),

Here’s another very nice one that superimposes the pathway onto a simplified brainstem drawing (nice for the anatomical relations):

https://webeye.ophth.uiowa.edu/eyeforum/cases-i/case252/Fig2-INO-LRG.png

Source article:

https://webeye.ophth.uiowa.edu/eyeforum/cases/252-internuclear-ophthalmoplegia.htm

To see even more, try google image search on “medial longitudinal fasciculus”:

https://www.google.com/search?q=medial+longitudinal+fasciculus&tbm=isch

endochondral1  what is A and B in this pic? i knew it was dorsal pons ipsilateral but i just didn't know what part that was on the pic? +  
nwinkelmann  A and B are the superior cerebellar peduncles.http://what-when-how.com/wp-content/uploads/2012/04/tmp15F2.jpg +  


submitted by usmleuser007(128),

1) Superficial (first-degree) = Epidermis ~ presents as red skin without blisters

2) Superficial partial thickness (second-degree) = Extends into superficial (papillary) dermis ~ Presents with redness with clear blister & blanches with pressure

3) Deep partial thickness (second-degree) = Extends into deep (reticular) dermis ~ presents as yellow or white skin with less blanching. May be blistering.

4) Full thickness (third-degree) = Extends through entire dermis ~ presents as stiff and white/brown skin. No blanching.

5) Fourth-degree = Extends through entire skin, and into underlying fat, muscle and bone ~ presents as black skin; charred with eschar

endochondral1  what is rhus dermis? +1  
endochondral1  nvm its urshiol +  
btl_nyc  Allergic contact dermatitis because of contact with poison ivy. +  


submitted by usmleuser007(128),

1) Superficial (first-degree) = Epidermis ~ presents as red skin without blisters

2) Superficial partial thickness (second-degree) = Extends into superficial (papillary) dermis ~ Presents with redness with clear blister & blanches with pressure

3) Deep partial thickness (second-degree) = Extends into deep (reticular) dermis ~ presents as yellow or white skin with less blanching. May be blistering.

4) Full thickness (third-degree) = Extends through entire dermis ~ presents as stiff and white/brown skin. No blanching.

5) Fourth-degree = Extends through entire skin, and into underlying fat, muscle and bone ~ presents as black skin; charred with eschar

endochondral1  what is rhus dermis? +1  
endochondral1  nvm its urshiol +  
btl_nyc  Allergic contact dermatitis because of contact with poison ivy. +  


submitted by meningitis(162),

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +1  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +  


submitted by meningitis(162),

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +1  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +  


submitted by usmleuser007(128),

This more likely to be diuretics rather than laxatives b/c

the lab study shows a renal dysfunction (BUN & Creatinine are elevated)

Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis

endochondral1  would laxatives also have the low potassium? +1  
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken? +  
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis. +  
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis. +1  
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue. +  


Premie has no surfactant

Angiotensin II - generated in hypovolemia

Dipalmitoyl lecithin aka dipalmitoylphosphatidylcholine lung surfactant

Phosphatidylinositol 4,5-bisphosphate aka PIP2 Gq receptor pathway

Phosphatidylserine -involved in intrinsic apoptosis when exposed on extracellular surfaces

Sphinogmyelin - composes myelin and also has roles in signal transduction, apoptosis. Lecithin: Sphingomyelin ratio >2 indicates mature fetal lungs.

endochondral1  how are we supposed to know that dipalmitoyl lecithin is the same thing as dipalmitorylphosphatidylcholine +1  


submitted by hayayah(418),

The damage is in the L midbrain in the area affecting the corticospinal tract. Because it is in the midbrain, decussation in the pyramids (medulla) so it will show ipsilateral dysfunctional motor signs.

Photo of midbrain and important areas: shorturl.at/myHLR

masonkingcobra  Just for clarification, on the left side, you see where he had the infarction 7 years ago and the tissue is gone. +1  
chefcurry  so is the dysfunction on the contralateral side? +  
praderwilli  If the decussation is in the pyramids of the medulla, shouldn't it be contralateral hemiparesis if the damage is on the right? It confuses me because of the labeling right and left at the top of the pictures. +  
endochondral1  that link isnt working @ hayayah....is there any good picture to look at to know where the tracts are on this section? +  


submitted by xxabi(98),

Swelling of the cell (e.g., hydropic degeneration): tissue ischemia → decreased ATP production → decreased Na+/K+ ATPase and Ca2+pump activity → diffusion of Na+ and water into the cell → cellular swelling

endochondral1  can someone explain how to cross out the other choices> +1  
endochondral1  what is hydropic degneration and where do i learn about it? why is it not the loss of plasma membrane integrity? +1  
shaeking  Endochondral1, I had the same question. I tried figuring it out and this is what I came up with. The CHF and congestion of the lungs is reducing the amount of oxygen getting to the renal cells. With hypoxia there is decreased aerobic resp in mitochondria with decreased ATP. Without ATPase Na builds up and water follows. As far as the loss of membrane integrity. I think it would cause cellular destruction not just hydropic changes. This is my best guess. +1  
charcot_bouchard  Membrane damage is irreversible stage of cellular injury. if membrane is damaged cell is dying & it will shrink. or totally destroyed by inflammation. they are specifically asking hydropic changes ie cellular swelling. which is the 1st sign of reversible cell injury due to failure of Na/K pump +  
winelover777  @endochondral1 Chapter 1 of Pathoma. Also FA 2019 p207 describes hydropic degeneration without saying those exact words in the first bullet under reversible cell injury. +  


submitted by xxabi(98),

Swelling of the cell (e.g., hydropic degeneration): tissue ischemia → decreased ATP production → decreased Na+/K+ ATPase and Ca2+pump activity → diffusion of Na+ and water into the cell → cellular swelling

endochondral1  can someone explain how to cross out the other choices> +1  
endochondral1  what is hydropic degneration and where do i learn about it? why is it not the loss of plasma membrane integrity? +1  
shaeking  Endochondral1, I had the same question. I tried figuring it out and this is what I came up with. The CHF and congestion of the lungs is reducing the amount of oxygen getting to the renal cells. With hypoxia there is decreased aerobic resp in mitochondria with decreased ATP. Without ATPase Na builds up and water follows. As far as the loss of membrane integrity. I think it would cause cellular destruction not just hydropic changes. This is my best guess. +1  
charcot_bouchard  Membrane damage is irreversible stage of cellular injury. if membrane is damaged cell is dying & it will shrink. or totally destroyed by inflammation. they are specifically asking hydropic changes ie cellular swelling. which is the 1st sign of reversible cell injury due to failure of Na/K pump +  
winelover777  @endochondral1 Chapter 1 of Pathoma. Also FA 2019 p207 describes hydropic degeneration without saying those exact words in the first bullet under reversible cell injury. +