Phys 3 + 4 Flashcards
How is K+ reabsorbed?
paracellularly
What does an increased flow rate mean for K+?
enhances secretion because the concentration build up doesn’t occur until later on because the concentration is diluted…there’s more Na+ in the later parts of the nephron, which leads to its reabsorption and K+s secretion
What does a decreased flow rate mean for K+?
the concentration builds up earlier, and without the gradient secretion slows
What is an important role of flow rate when Na+ levels increase?
aldosterone is down regulated, so increased flow rate (caused by increased GFR and decreased PCT Na+ reabsorption) helps to maintain levels of K+ excretion
What does chronic acidosis do?
stimulate K+ secretion
*acute decreases excretion
What’s the biologically active form of vitamin D called?
calcitriol
What is the role of calcitriol?
resorbs bone by stimulating osteoclasts–>increased Ca+ and phosphate plasma concentrations
What does calcitriol do to bone? intestine? kidney?
- promotes osteod mineralization; osteoclast mediated resorption
- increases Ca2+ and phosphorous absorption
- increased phosphorous and Ca2+ reabsorption
*works with PTH
What receptor does calcitriol use?
VDR (found throughout body)
What is the role of calcitonin?
- lowers serum Ca2+ and phosphate by inhibiting bone resorption (decreases activity/number of osteoclasts)
- promotes renal excretion of Ca2+ and phosphate
*works against PTH
What does calcitonin do to bone? kidneys?
- inhibits osteoclast bone respiration
- promotes phosphate and Ca2+ excretion
*used to treat osteoporosis, Paget’s disease, HyperCa2+
What does PTH do to bone? intestine? kidneys?
- increase osteoclast resorption
- Increase Ca2+/Pi absorption indirectly via calcitriol production
- increase reabsorption of Ca2+ (mainly in DCT); decreased–>reabsorption of Pi in PCT, Na+/H+ anti porter, and bicarbonate reabsorption
What can be caused by excessive PTH?
hypercalcemia, hypophosphatemia, hypercholermic metabolic acidosis
When is CaSR activated?
high levels of Ca2+
*inhibits Ca2+ reabsorption on apical membrane
How is Ca2+ reabsorbed in the PCT?
mainly paracellular (some trans cellular–>Ca2+ ATPase and Na-Ca2+ anti porter)
*major site
What does volume contraction do to Ca2+ reabsorption?
increases it
Why is active transport needed for Ca2+ in the DCT?
because there is a negative transepithelial voltage
*TRPV5 is used to reabsorb Ca2+
What four things can activate TRPV5? what can inhibit it?
- PTH, Vit D, Calcitriol, Thiazide diuretics; Alkalosis
2. Acidosis
How does Pi cross the membrane in the PCT?
via it’s own, unidentified transporter and via the Na+/Pi symporter
How is Vit. D activated in the Kidney?
1 alpha-hydroxylase/CYP1alpha/renal 1 alpha hydroxylase activates it in the PCT
How do the following regulate Pi levels: FGF-23, PTH, Calcitriol, Insulin, Dietary, renal function?
- increase excretion
- increase excretion
- increase absorption
- lowers serum levels via cell uptake
- variable
- decrease reabsorption (bc no Vit. D)
What is the most important hormone that regulates Pi excretion?
PTH
*inhibits Na+/Pi transporters and Na/H antiporter in apical membrane of PT cells
How does chronic acidosis affect Pi excretion? alkalosis?
- increase
2. decrease
Where does Mg fine tuning take place?
DCT
*crosses apical border via TRPM6
