Part Tres--Electrolyte Balance & Acid/Base Buffer Flashcards
___% of total body K+ is intracellular (recall the role of the Na+-K+-ATPase)……Normal plasma [K+] = __ mEq/L:
98%…4 mEq/L
What can high [K+] do to resting membrane potential and therefore excitability of the cell?
high [K+] = lower resting membrane potential = increased excitability
How do we NOT DIE after eating a banana? (2 ways :))
- RAPID uptake of K+ into the cells (aldosterone, insulin, eli) 2.Slower renal excretion
‘Obligatory’ reabsorption of approx 90% of the filtered load of K+ in the ________ and the ___________.
proximal tubule….thick ascending limb
How is the physiologic regulation of renal K+ excretion primarily achieved?
By SECRETING into the LATE distal and collecting tubules (OPPOSITE mechanism from Salt and Water)
How do I find FL (filtered load)?
GFR x Amount of Substance in body
Since K+ is secreted late in the game what are the three transporters used? Also, what is driving the charge difference?
- Na+/K+ pump (BL membrane) 2.K+ channels (L membrane) 3. K+/Cl- cotransporters (L membrane)….Na+ reabsorption at this stage is promoting a negative environment (thus promoting K+ secretion)
What do we do when we have K+ depletion? (name some transporters for me)
- Energy dependent K+/H+ antiporter (L membrane) 2.K+ selective channels (BL membrane)
What does a hypertonic extracellular environment result in K+ levels in the blood?
HyperKalemia
What does cell lysis do to plasma levels of K+?
HyperKalemia (exercise-induced muscle breakdown)
What is the relationship between ECF [H+] and Plasma [K+]?
Parallel…increase in ECF [H+] = increase in plasma [K+]…vis versa
Metabolic acidosis due to ________ (HCl, H2SO4) increases plasma K+ to a much greater extent than a similar acidosis produced by __________ (lactic acid, keto acids)
inorganic acids….vs…..organic acids
How does respiratory acidosis/alkylosis affect plasma [K+]?
little to no effect :)
What are the two ways the body works to secrete a high [K+] ECF?
Increase Na+/K+ action on the distal nephron cells 2.increase aldosterone secretion (also increases Na+/K+ action AND increases luminal K+ permeability
What does increased tubular flow do to K+ secretion?
increases secretion (1.c/o low tubular fluid [K+] 2.more Na+ reabsorption and more Na+/K+ activity)
What can loop diuretics do to plasma [K+]?
can cause HypoKalemia (1.less reabsorption 2.more secretion (Na+/K+ pumps goin crazy!)
What are the three ways the body combats hypoCalcemia?? how does the kidney connect to the G.I. tract here?
1.Kidney (more to come) 2.G.I. absorption (renal Vit-D activation!!) 3.bone resorption
Which part of the kidney does PTH target? What are the 2 outcomes? Which membrane?
PTH acts on the distal tubule…1) Ca2+ ATPase (BL) 2)Na+-Ca2+ exchanger(BL)
How is the problem of hyperPhosphatemia solved during bone resorption? WHERE does this happen?? Which transporter is involved???
PTH inhibits Renal HPO42- reabsorption….PROXIMAL TUBULE….the Na+/HPO42- cotransporter on the L membrane is BLOCKED! thus we’ll pee it on out
H+ balance: note that concentrations are expressed in _____ Eq “Normal” pH range: ____ - ____ Survival limits: ____ - ____.
7.37 - 7.42…….6.80 - 8.00
What are the two sources for H+ accumulation? What is the release for both?
1.Volatile- oxidative metabolism…2. Fixed-AA metabolism
What are the two main ways fixed metabolism causes a build up of acid?
1.exercise (lactic acid) 2. DM
How do we get rid of volatile acid?
respiration
Which is more prevalent volatile or fixed acid?
Volitile is 5,000x more prevalent in the body
What are the three lines of defense against fixed acid accumulation in the body?
1.Physiochemical Buffering (H2PO4, HCO3) 2.Respiratory compensation 3.Renal compensation