K+ and Ca2+ (Muster) - W2 Flashcards
where is K+ primarily stored?
What could deplete those stores?
- 98% intracellularly
- burns
- crush injuries
- reperfusion injuries
How does insulin affect K+?
- insulin increases Na-K ATPase
- promotes skeletal and muscle uptake
- eat –> insulin –> alleviates K+ serum
How do catecholamines affect K+?
- bind to B2 receptors
- stimulate the Na-K ATPase inducing cellular uptake
- likely permissive at baseline
How does plasma concentration of K+ affect uptake?
- serum K+ rises –> cellular uptake increased
How does exercise affect K+?
- muscle cells release K+
- related to degree of exercise
How does pH affect K+
- K+ rises in serum.
What happens with tonicity and K+?
- hyperglycemia
- water and K+ leave the cell
- more water than K+ leaves
- K+ inside cell reduces Na-K ATPase
What do you give to prevent arhythmia and cardiac arrest with high potassium?
- Ca2+
along w/insulin and glucose
What is the control of potassium:
proximal tubule
thick ascending limb
principle cell of collecting duct
- proximal tubule = 55-65% via tight junctions
- thick ascending limb = 25%
- principle cell = 10%
What are the 4 stimuli for K+ secretion (and therefore excretion)
-
sodium delivery to distal convoluted tubule
- more sodium = more K+ excretion
- increased flow rates
- higher flow = higher gradient stimulating movement into the lumen
-
plasma levels of K+
- increased activity of ATPase w/higher levels
-
aldosterone
- increases ENAC
- increases ROMK
- increases NA-K ATPase
What 2 things can stimulate aldosterone and what happens with each?
- Angiotensin II system
- used for NA+ retention
- stops ROMK channel
-
serum potassium
- increases ROMK in membrane
- less stimulus for ang II
What are the stimuli for BK channel?
- increased FLOW
- increased EC potassium
How is K+ reabsorbed?
- occurs in Alpha and beta intercalated cell
- K+ is exchanged for H+
- lots of H+ must be processed to reabsorb K+
- active process!!
- also requires reabsorption of bicarbonate
Describe the availability of calcium
- 40-50% is bound to ALBUMIN
- 10% BOUND to citrate, phosphate
- 50% is available as ionized calcium
How much calicum is aborsbed in each part of the loop?
- proximal tubule = 60-70%
- thick segment = 20%
- convoluted tubule = 10%
- collecting duct = 5%
By which process is most of the calcium reabsorbed?
- paracellular (85%)
How is calcium reabsorbed in the thick ascending limb?
-
calcium sensing receptor
- binds free calcium
- when stuff isn’t bound, upregulates calcium reabsorption
- bound = claudins can stop paracellular reabsorption of calcium
How is calcium reabsorbed in the distal convoluted tubule and cortical collecting duct?
- enters through TRPV5 channels
- most is transcellular
- binds to calbindin to carry it to the other side of the cell.
- Na+/Ca2+ antiporter allows it into the capillary.
- 3Na in to 1Ca out.
- PTH can upregulate TRPV5 for increased uptake on luminal side and increased excretion on back side.
When is PTH released?
- PTH is released when all calcium receptors aren’t bound.
- low ionized calcium stimulates PTH release.
What does PTH do to bone?
- stimulates IMMEDIATE release of stored skeletal calcium
- LONG TERM
- stimulates bone reabsorption
- acts on cortical bone
- also releases phosphorus
What does PTH do to the gut?
- increases calcium and phosphate reabsorption by increased 1,25 vitamin D
What does PTH do to the kidney?
- increases the production of vitamin D in the proximal tubule
- increases renal Caclium reabsorption
- stimulates renal phosphorus excretion - phosphorus wasting.
