Clara Cell vs Type II Pneumocyte

[Cliff Huxtable]

What is the difference between the two in terms of regenerating cells?

Clara cells "act as reserve cells"

and

Type II Pneumocytes "proliferate during lung damage"

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[Mortal_Lessons]

What is the difference between the two in terms of regenerating cells?

Clara cells "act as reserve cells"

and

Type II Pneumocytes "proliferate during lung damage"

According to Wheater's, type II pneumocytes retain the capacity for cell division and can differentiate into type I pneumocytes in response to damage to the alveolar lining. Also the pneumocytes line the alveoli and are not present proximally in the respiratory bronchiole. Clara cells act as stem cells (i.e. they are able to divide, differentiate and replace other damaged cell types.) and are located in the respiratory bronchioles. Are Clara cells even present in the alveoli, or is their predominance limited to the respiratory bronchiole just prior to them blossoming into alveoli?

 

[Cliff Huxtable]

Another question:

Could someone explain this to me:

"At the peak of inspiration, lung volume is FRC + one TV"



Also, why is intrapleural pressure slightly negative at FRC and not 0 ?

And why do inspiration and forced expiration INCREASE pulmonary vascular resistance?

THANKS!

 

[SnowTown]

Another question:

Could someone explain this to me:

"At the peak of inspiration, lung volume is FRC + one TV"



Also, why is intrapleural pressure slightly negative at FRC and not 0 ?

And why do inspiration and forced expiration INCREASE pulmonary vascular resistance?

THANKS!

"At the peak of inspiration, lung volume is FRC + one TV"

that's just the definition of what it is? if you look on page 476 of 1st aid (2009) peak inspiration is FRC + tidal vol

intrapleural pressure is pretty much always negative because of the tug of war between the chest wall and the lung

not sure about the pul vascular resistance one... maybe inspiration and expiration both compress on the lung and thus it's vasculature a little??? again, i don't know about this one, just guessing.

 

[Cliff Huxtable]

Oh, I figured the peak of inspiration should incude the IRV.

 

[future_dr_house]

I'm gonna throw up a guess for the pulmonary vascular resistance

No matter what, the flow rate in the pulmonary vasculature (Q) must equal the flow rate of the heart (CO). If there is a mismatch then you get fluid in the lungs.

Q = deltaP/R (an equation you should be familiar with by now)

As we inspire the change in pressure increases and in order to maintain the same flow rate, PVR must increase.

Normally expiration is passive, but if we start using muscles, now you can imagine the diaphragm and intercostals pushing on the lung parenchyma to expire more quickly, this increases the change in pressure (albeit in the opposite direction so there will be a minus sign) and again, the PVR must increase.

 

[sgod34]

"At the peak of inspiration, lung volume is FRC + one TV"

I think this is because at the peak of a normal/quiet inspiration, you are at the peak of TV, since TV is the air that your fills lungs during regular inspiration. Also, at normal inspiration your total volume includes ERV and RV. This is because ERV only decreases in forced expiration, not normal expiration. And RV is constant and will not change with any type of breathing. Therefore, FRC doesn't change at all during quiet breathing, and it will stay constant during expiration and Inspiration. At rest (right before you start inspiration), FRC = lung volume. So basically, when you take a normal breath your volume = TV (the volume you are inspiring, about 500 mL) + FRC (FRC = ERV+ RV; the volume that is in your after a normal expiration).

Also, why is intrapleural pressure slightly negative at FRC and not 0 ?
I'm not positive, but I think it's because your lungs have a tendency to collapse inwards, while the chest wall wants to expand. At FRC, the inward pull by your lungs is equal to the outward pull of your chest wall. This makes airway pressure atmospheric, 0. However, a negative intrapleural pressure is created due to the equal, but opposing pressures in the lungs.

And why do inspiration and forced expiration INCREASE pulmonary vascular resistance?
Pulmonary vaculature resistance is increased in inspiration and expiration because of the increased volume seen after the start of a TV. It is minimum only at FRC level, when your TV=0. Any deviation of volume from FRC (inspiration or expiration) will increase pulmonary vacular resistance.

 

[Cliff Huxtable]

Thank you so much, SDN FTW!

 

[SnowTown]

Oh, I figured the peak of inspiration should incude the IRV.

yeah, i'll probably think that too if i ran into a question like that without reading this thread

think they'll probably say peak of maximal inspiration if they're after the IRV

 

[Deferoxamine]

And whenever "Clara Cells" is one of the multiple choices, it is never the answer. Just sayin'.

 

[future_dr_house]

And whenever "Clara Cells" is one of the multiple choices, it is never the answer. Just sayin'.

unless it mentions anything about influenza A, then that's the only answer

 

[Deferoxamine]

unless it mentions anything about influenza A, then that's the only answer

🙁

future_dr_house: 1
Deferoxamine: 0

Thanks for playing.

 

[Cliff Huxtable]

Off topic:

What is a normal A-a gradient, <10mmHg or 10-15mmHg?

 

[NCF145]

off topic:

What is a normal a-a gradient, <10mmhg or 10-15mmhg?

10-15

 

[Cliff Huxtable]

So sorry but I am trying to tie up loose ends:

Why does exercise NOT change the PaO2 or the PaCO2?

 

[NCF145]

So sorry but I am trying to tie up loose ends:

Why does exercise NOT change the PaO2 or the PaCO2?

Because cells don't take O2 out of the arterial system until it reaches the capillaries. Both PaO2 and PaCO2 are calculated based on arterial measurments, which are before the capillaries. What you do get though is a decrease in mixed venous oxygen content and an increase in venous CO2. O2 and CO2 are both perfusion limited. When you excercise your CO increases, increasing your perfusion and maintaining PaO2 and PaCO2 levels.

 

[metallo]

Because cells don't take O2 out of the arterial system until it reaches the capillaries. Both PaO2 and PaCO2 are calculated based on arterial measurments, which are before the capillaries. What you do get though is a decrease in mixed venous oxygen content and an increase in venous CO2. O2 and CO2 are both perfusion limited. When you excercise your CO increases, increasing your perfusion and maintaining PaO2 and PaCO2 levels.

I had been wondering the same thing myself... thanks for the good explanation.

 

[Cliff Huxtable]

Why does Secondary Hyperparathyroidism due to renal disease present with LOW calcium but HIGH phosphate?

HIGH PTH and LOW vitamin D I understand.

 

[TMP-SMX]

A functional kidney is required to excrete phosphate and to contain the 1-alpha-hydroxylase to produce active Vitamin D. Despite the high PTH, there is little functional kidney to produce 1-alpha-hydroxylase. When you have low vitamin D, you have low calcium and phosphate because you aren't absorbing it from the GI tract. However, the problem is that PTH also has some function directly in the GI tract and phosphate is less Vitamin D dependent for its absorption. So not only do you have low calcium you have high phosphate from kidney disease, and therefore PTH increases making the cyclical problem worse. PTH releases both calcium and phosphate from the bone and only increases reabsorption of calcium and excretion of phosphate in the kidney with normal function. With poorly functioning kidneys, the excretion of phosphate is severely reduced. So more phosphate and more PTH.