Lecture 18: Renal Phys Con't Flashcards
relate chronic HTN to the AA’s ability to autoregulate with dilation/constriction
chronic HTN > continuous constriction of AA to prevent overperfusion > harder to dilate in cases where pt becomes hypotensive
(3) causes of hardening/calcification of vasculature
- chronic HTN
- oxidative stress
- uncontrolled diabetes
describe what overperfusion would look like past the upper limits of autoregulation
- AA would attempt to constrict to prevent overperfusion (but would not be enough)
- GC pressure would increase leading to:
+increased NFP
+very fast filtration rate
+very fast reabsorption rate
+massive UOP
describe what underperfusion would look like past the lower limits of autoregulation
- the AA would attempt to dilate to prevent underperfusion (but wouldn’t be enough)
- GC pressure would decrease leading to:
+slower filtration rate
+slower reabsorption rate
+reduced UOP
describe how a slow fitration rate impacts reabsorption rate:
since there is more time spent in the tubule, there is a larger percentage of filtrate being reabsorbed by the PT caps
if filtration rate is slow, there’s not good filtration happening (more reabsorption)
beta blockers, beta agonists, CCBs, & pressors all affect this arteriole more
affects AA more
angiotensin affects this arteriole more
EA
since creatinine is freely filterable, as it travels further into the PCT, what would the [creatinine] be?
the [creat] would be more concentrated the further along it travels the PCT (d/t more water getting reabsorbed)
how much water gets reabsorbed at the PCT after filtration?
2/3
under normal circumstances, the macula densa “counts” a normal amount of these ions that pass by it
Na+
Cl-
under these conditions:
* higher filtration rate
* normal amount of reabsorption
the amount of NaCl at the TAL would be:
the MD would “count” MORE NaCl at the TAL d/t the high GFR
if the kidney filters MORE but does not reabsorb MORE, the MD cells would count MORE NaCl at the thick ascending limb
under these conditions:
* lower filtration rate
* normal amount of reabsorption
the amount of NaCl at the TAL would be:
the MD would count a LOW number of NaCl at the TAL d/t the LOW GFR
if the kidney filters LESS but does not reabsorb LESS, the MD cells would count LESS NaCl at the thick ascending limb and the MD cells would increase AT II levels to increase GFR
under these conditions:
* normal filtration rate
* increased Na+ and Cl- reabsorption at the PCT
the macula densa would sense the GFR to be?
the macula dense would sense the GFR to be LOW due to a less than normal amount of Na+ being counted at the TAL and AT II would be secreted leading to a HIGHER GFR
ACE-i’s, ARBs would prevent this
SGLT transporters in proximal tubule transports how many glucose per how many Na+?
1:1
1 glucose INTO cell for 1 Na+ INTO cell
Na+ travels down its concentration gradient pulling in 1 glucose molecule with it
secondary AT
INTO cell from TUBULE
a large increase in tubular glucose would have the following effects on reabsorption and GFR:
- increase in tubular glucose = increase in SGLT transportation of glucose AND sodium into cell
- increased Na+ into cell = more Na+ reabsorbed
- more Na+ reabsorbed means LESS Na+ at MACULA DENSA
- low Na+ count at MD = increase in AT II = increase in GFR
what is hyperfiltration?
- “wear & tear” on the nephrons causes accelerated loss of nephrons
chronic uncontrolled DM + amino acid intake
how many amino acids get transported with the Na+/AA transporter?
1:1
1 amino acid INTO cell for every 1 Na+ INTO the cell
secondary AT
a large increase in amino acids would have the following effects on reabsorption and GFR:
- increase in tubular amino acids = increase in Na+/AA transportation of amino acids AND sodium into cell
- increased Na+ into cell = more Na+ reabsorbed
- more Na+ reabsorbed means LESS Na+ at MACULA DENSA
- low Na+ count at MD = increase in AT II = increase in GFR
apical side of the cell =
tubular side of the cell wall
basolateral side of cell
interstitial fluid side of cell wall
list the basolateral transporters on a PCT cell:
- GLUT transporter (facilitated diffusion)
- Na+/K+/ATPase pump (primary AT)
list the apical co-transporters on a PCT cell:
- SGLT (secondary AT)
- Na+/AA (secondary AT)
list the basolateral antiporter on a PCT cell:
Na+/K+/ATPase pump
list the antiporter on the apical side of the PCT cell:
- NHE (sodium/hydrogen exchanger)