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Welcome to geekymle’s page.
Contributor score: 9


Comments ...

 +0  (nbme18#10)

what i dont understand of this question is that why is cystic fibrosis causing hyperinflated lungs?

spartanmd  I believe the decreased clearance of respiratory secretion causing difficulty to exhale and air trapping. Chronic air trapping causes hyperinflation of the lungs and clubbing of the hands. +

 +0  (nbme18#30)

okay. i get this question, but what i dont understand is that why cant we inform the patient of the health consequences of not treating her condition?


 +1  (nbme19#41)

Surfactant deficiency → no reduction of alveolar surface tension → reduced pulmonary unfolding → lungs wont open up → decreased lung compliance and functional residual capacity → hypoxemia and hypercapnia

this should help


 +2  (nbme16#50)

i tried but i'm not able to reason this question. can anyone please help me on this?

sunnyd  I found a good explanation in the discussion here: https://forums.studentdoctor.net/threads/nbme-16-help.1059939/page-2 +1
geekymle  thank you! it was the wording of the question which got me!! +1
andro  I think there were two possible ways of approaching this. The first was by appreciating that the tumor cells ( which release Growth Hormone ) would express growth hormone releasing hormone receptors GHRH receptors - GHRH uses the Gs signalling pathway ( Net effect an increase in cAMP from the increased activity of adenyl cyclase ) The second and more straight forward approach From the stem of the question already they told us we are dealing with an overactivation of the G alpha stimulatory subunit . If the GTPase aint working ( meaning it cant be inactivated ) , the effect would be an increase in the activity of adenyl cyclase +5
meryen13  well I know you guys probably thought its a jam kinase because of somatotroph adenoma. we know growth hormone has a jar/ kinase right? but the question was really sneaky and mentioned that there is a G alpha s subunits protein!! that should remind you that Gs activates adenylyl cyclase to increase CAMP. the key world was Gs (and I didn't think about it cause I just saw somatotropin adenoma) +
m0niagui  where in FA2020 will I find reference to this? I'm still at a loss ;/ +1
kard  m0niagui, Just Get this GHRH (Gs)cAMP ---->GH(Jak/STAT), And you can check all of them on the "Signaling Pathways of Endocrine Hormones" +1




Subcomments ...

submitted by azibird(177),

Endothelin (ET)-1, a potent vasoconstrictor peptide from vascular endothelial cells, is also synthesized and secreted by cardiomyocytes and induces hypertrophy of cardiomyocytes through activating phospholipase C, protein kinase C, extracellular signal-regulated kinase (ERK) 1 and ERK2, and upregulation of c-Fos and c-Jun.

https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000112596.06954.00?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

motherhen  is this super out of left field or am I supposed to know this +10  
ab721  @motherhen I don't know if this is correct, but I personally tried to reason this one out. If hypertrophy is occurring, more sarcomeres are added which means more beta-myosin. Hypertrophy also means the cell is doing more work, so a transcription factor is likely to be upregulated. From there, the only option with both of those increased had endothelin increased as well, though unclear why that's necessarily increased. +5  
motherhen  genius +1  
yerpderp  Loud S2 made me think of pulmonary hypertension which would have an incr endothelin +1  
geekymle  that loud s2 was from systemic hypertension. +  
utap2001  systemic hypertension -> induce LV hypertrophy -> induce pulmonary hypertension -> endothelin increase, plus loud S2 and S4 gallop +  


This question is worded extremely poorly-- Basically I looked at it as if 1) the twin studies showed that it was 50% genetic 2) the other studies only found loci accounting for a small percent of that heritability

Based on 1 & 2 you can get to the answer

dhpainte22  This question was there just to annoy people and their train of thought basically during the exam :( +1  
geekymle  it did trouble me but i somehow managed to get it right, but kept coming back to it again n again to understand what exactly it was trying to ask. +  


submitted by geekymle(9),

i tried but i'm not able to reason this question. can anyone please help me on this?

sunnyd  I found a good explanation in the discussion here: https://forums.studentdoctor.net/threads/nbme-16-help.1059939/page-2 +1  
geekymle  thank you! it was the wording of the question which got me!! +1  
andro  I think there were two possible ways of approaching this. The first was by appreciating that the tumor cells ( which release Growth Hormone ) would express growth hormone releasing hormone receptors GHRH receptors - GHRH uses the Gs signalling pathway ( Net effect an increase in cAMP from the increased activity of adenyl cyclase ) The second and more straight forward approach From the stem of the question already they told us we are dealing with an overactivation of the G alpha stimulatory subunit . If the GTPase aint working ( meaning it cant be inactivated ) , the effect would be an increase in the activity of adenyl cyclase +5  
meryen13  well I know you guys probably thought its a jam kinase because of somatotroph adenoma. we know growth hormone has a jar/ kinase right? but the question was really sneaky and mentioned that there is a G alpha s subunits protein!! that should remind you that Gs activates adenylyl cyclase to increase CAMP. the key world was Gs (and I didn't think about it cause I just saw somatotropin adenoma) +  
m0niagui  where in FA2020 will I find reference to this? I'm still at a loss ;/ +1  
kard  m0niagui, Just Get this GHRH (Gs)cAMP ---->GH(Jak/STAT), And you can check all of them on the "Signaling Pathways of Endocrine Hormones" +1  


submitted by cassdawg(1101),

This ratio is used to determine appropriate production of lung surfactant, so this baby would not have appropriate production of surfactant if birthed at the time of the ratio calculation. It would go into neonatal respiratory distress syndrome.

TL;DR: surfactant decreases lung recoil, so the lack of surfactant in this baby will cause an increased recoil which will decrease the functional residual capacity (FA 2020 p661-662)

Surfactant is necessary to decrease surface tension of alveoli and increase compliance of the lungs (remember when the lungs have greater compliance, this makes the lungs easier to fill). Surfactant also helps to prevent alveolar collapse as the lack of surfactant allows there to be varying surface tensions between large and small alveoli (Law of Laplace), so lack of surfactant would lead to widespread atelectasis (alveolar collapse). Because surfactant serves to decrease these forces which normally favor collapse of the lung, it also serves to decrease the lung recoil.

Lack of surfactant in a baby = increased alveolar surface tension, lower compliance, more alveolar collapse, more recoil (less residual volumes)

Total lung capacity is unchanged because with enough force you can still expand the lungs to full capacity.

geekymle  hey ya! thanks for the explanation, but i'm still not able to understand why decreased functional residual capacity. +1  
cassdawg  Not sure if this will help but another way of thinking of this is that it is similar to pulmonary fibrosis with decreased compliance leading to lower functional residual capacity! The only difference is here you retain total lung capacity because it is a "reversible" compliance issue (give them surfactant) and the lungs themselves are not the issue. Also, like you said in your comment, lungs won't open up so there is a lower starting point for breathing, and thus a lower functional residual capacity (volume left in the lungs after normal expiration). +2  


submitted by cassdawg(1101),

Water does not require transport proteins or energy for absorption, and transepithelial transport means it must go through the epithelial cells. C is the best match.

geekymle  i dont know why i missed it. it was a direct answer! +1