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This makes sense, thanks!
I was able to break it down to diuretic or alcohol use and chose alcohol use under the assumption that the patient's serum Cl- levels were low (90; N = 95-105) since Cl- is also lost with vomiting. Im assuming that it was wrong for me to make the association between alcohol use and vomiting.
@dysdiadochokinesia I think we can rule out alcohol use by looking at our patient's history and demographic. A 16yo girl who is dieting and constantly studying probably isnt getting turnt because 1) alcohol has empty calories (defeats the point of dieting), 2) why would you try to study when you're drunk, 3) where will this 16yo in social isolation get alcohol
why not membrane receptor?
delF508 is a 3 base pair deletion of phenylalanine at amino acid position 508. Mutation causes impaired post-translational processing of CFTR (improper folding) which rough ER detects. Sends mutant misfolded CFTR to the proteasome for degradation, preventing it from reaching cell surface. So problem is not malfunctioning CFTR channels in the surface; problem is complete absence of CFTR on cell surface (since they keep getting misfolded and sent to proteasome to be trashed). Source of primary problem: error in protein structure
@Is3076 because the CFTR is a channel not a receptor.
FA 2019 p. 60
@a1913 is correct- as for @angelaq11, you can still have a receptor that also functions as a channel as they are not mutually exclusive. An example of this is the nAChR found on postsynaptic NMJ neurons. This is a non-selective, ligand-gated, ionotropic receptor that functions as a channel once its ligand (i.e., ACh) has bound to the active site to induce conformational change. Similarly on the same realm: CFTR is an ionotropic receptor that concurrently functions as a Cl- channel once its ligands (ie. 2 ATP) is bound to open the channel and enable Cl- flux.
This question in particular is asking for the underlying pathophysiologic mechanism for cystic fibrosis, which boils down to an issue with the primary structure of a protein resulting in its misfolding and subsequent sequestration/degradation.
could be due to increased blood volume leading to secretion of ANP and thus natriuresis which would normalize serum sodium levels?
that's the only reason I could think of
My guess is that the sodium and water loss from 21a-hydroxylase deficiency would result in increased RAAS activation and production of Angiotensin II (AGII). Recall that AGII affects the PCT by upregulating Na/H+ exchangers, allowing for there Na/H2O to be resorbed, thus partially counteracting the impact of aldosterone deficiency at the collecting duct. However, I'm not sure if the effect of AGII on the PCT is great enough to entirely counterbalance the loss of aldosterone to present with normal sodium levels.