Unit 7 - Regulation of Potassium Flashcards Preview

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Flashcards in Unit 7 - Regulation of Potassium Deck (28)
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1

how is K+ related to H+?

[K+] participates in pH regulation, due to effective K+/H+ exchange across cell membrane

2

extracellular VS intracellular K+ concentrations

extracellular: 3.5-5.0 mM
intraceullar: 120 mM (98% of total body K+)

3

how is K+ related to the cell voltage?

major determinant of cell voltage of [K+] gradient
-if extracellular K+ increases, the gradient decreases, so voltage depolarizes (less negative)
-if intracellular K+ increases, gradient increases, so hyperpolarizes (more negative; this is what it is usually)

4

how is K+ important in excitable and unexcitable cells?

K+ gradient across cell membrane is major determinant of potential in both types of cells
-in excitable (cardiac, neural, muscle), the currents are central to property of "excitability"

5

what defines hyperkalemia?

plasma [K+] above 5.0 nM
-decreases outwardly directed K+ gradient
-resting membrane potential is depolarized
--muscle hyperexcitability
--cardiac conduction disturbances (ventricular arrythmia and fibrilation, tachycardia)
-metabolic acidosis (since K+ enters cells, H+ exits cells)

6

what defines hypokalemia?

plasma [K+] below 3.5 mM
-increases outwardly directed K+ gradient
-resting membrane potential is hyperpolarized
--muscle hypoexcitability
--cardiac pacemaker disturbance (arrythmia, bradycardia)
-metabolic alkalosis (since K+ exits cells, H+ enters cells)

7

K+ balance and distribution throughout body (external VS internal VS kidney) daily

external: GI uptake (100 mmol)
-10 mmol in feces
-90 mmol to ECF

internal: ECF constant at 65 mmol (4.5 mM); exchange with organs
-muscle: 2600 mmol
-liver: 250 mmol
-bone: 300 mmol
-RBC: 250 mmol

kidney: 90 mmol excretion = 810 mmol filtration + 50 mmol secretion - 770 mmol reabsorbtion

8

what is the first line of defense against hyperkalemia? what is the one cell that doesn't participate in this?

increased uptake of [K+] into cells
-acute increase in plasma [K+] triggers release of insulin (pancreatic beta cells), epinephrine (adrenal medulla chromaffin cells), and aldosterone (adrenal cortex glomerulosa cells)
-these all act to activate K+/N+ ATPase, such that K+ can enter cells and Na+ can exit cells

since RBC don't have a nucleus or the ability to respond to the above hormones, they don't participate in this response

9

how is hyperkalemia related to diabetes?

since insulin is released in response to acute increases in [K+], poorly-controlled BM may compromise tolerance of diabetes patients to K+ load, and predispose them to hyperkalemia

10

why does acidemia cause hyperkalemia?

acidemia inhibits the Na/K ATPase and Na/K/2Cl cotransporters, which lowers intraceullar [K+] and causes K+ loss from cells
-also, H+ enters cells and K+ exits cells via K+/H+ antiport

11

how does alkalemia stimulate hypokalemia?

alkalemia stimulates Na/K ATPase and Na/K/2Cl cotransporters, so more uptake of K+ into cells, causing hypokalemia

12

how does the body handle K+ after an acute K+ load?

plasma K+ will slowly decrease back to baseline due to:
-initially high net cumulative translocation of K+ into cells (slowly tapers off)
-slowly increasing cumulative renal excretion of K+ above baseline

13

how does K+ reabsorption in proximal tubule change at low, normal, or high plasma K+ levels? in the distal tubule?

PT: IT DOESN'T; reaborption is constitutive (not regulated) in proximal tubule
-it's always most of the filtered K+ (~80%)

DT: either reabsorbs or secretes K+, depending on K+ balance and plasma K+ levels

14

K+ handling when dietary K+ intake is low and K+ balance is negative

-80% reabsorbed in proximal tubule constitutively
-10% reabsorbed in TAL constitively
-since low K+: 2% reabsorbed in collecting tubule + 6% reabsorbed in medullary collecting duct
-remainder: 2% of filtered load is remaining for excretion

15

what is an instance where hypokalemia can result, despite compensating increase in K+ reabsorption by distal nephron?

chronic dietary K+ deficiency

16

K+ handling when dietary K+ intake is high and K+ balance is positive

-80% reabsorbed in proximal tubule constitutively
-10% reabsorbed in TAL constitively
-since high K+: instead of reabsorption, there can be 20-180% K+ secretion at collecting tubule
-20-40% can be reabsorbed in medullary collecting duct
-remainder: 10-150% of filtered load remaining

17

how is K+ reaborption in proximal tubule?

paracellular, by 2 methods
-early PT: solvent drag (due to H2O entering paracellularly)
-late PT: since the voltage increases from negative (early) to positive (late), there is a driving force for the K+ to enter lumen paracellularly

18

how is K+ reabsorption in TAL?

both transcellular and paracellular
-since there is a positive voltage (due to PT actions), K+ and Na+ are driven across paracellularly
-Na+/K+/2Cl- co-transport on luminal side brings all into cell
--Cl-, K+ channels send through basolateral membrane, while Na+/K+ ATPase sends Na to blood, and K+ in
-K+ channel on luminal membrane sends K+ into lumen if need be

19

where does furosemide act?

on the TAL
-it inhibits the transcellular Na/K/2Cl cotransport on the luminal side, keeping Na+ and K+ in tubular lumen

20

mechanism of K+ reabsorption by distal nephron

transcellular
-there is an H+ pump to the luminal side, then a K+/H+ exchanger pump that sends K+ into cell and H+ out
-for every H+ exiting the cell, an OH- left in cell binds to CO2 to make HCO3-
-HCO3-/Cl- exchanger, Na/K ATPase, K+ and Cl- channels in basolateral membrane

21

why can hypokalemia cause secondary metabolic alkalosis?

there is increased reabsorption of k+ mediated by increased luminal membrane K+/H+ exchange
-the H+ secreted into lumen leaves behind OH- in cell to bind to CO2 and make HCO3-
-the HCO3- exits via HCO3/Cl antiport to cause alkalosis

22

mechanism of K+ secretion by distal nephron; what is it dependent on? what happens if furosemide is used?

transcellularly, and dpendent on flow and Na
-increased flow causes increased K+ secretion, pulling it forward
-if furosemide is used, Na+ hasn't been reabsorbed in TAL, so Na+ is absorbed here, and K+ secretion increases (hypokalemia)

23

how is tubular fluid flow related to distal tubule K+ secretion in high, normal, and low K+ diets?

no matter the diet, there will be increased K+ secretion with increased distal flow
-if high K+ diet, there is slower flow
-if low K+ diet, there is faster flow

24

regulation of K+ excretion at high dietary K+

1. increased distal nephron secretion of K+
-increased plasma [K+] increases uptake of K+ by basolateral membrane Na/K ATPase
-increased driving force for K+ transport across apical membrane
-increased synthesis and release of aldosterone by adrenal cortex
2. decreased distal nephron reabsorption of K+

25

how does aldosterone affect K+?

increases K+ secretion
-induces increased "capacity" for Na+ reabsorption and K+ secretion in distal nephron
-induces transcription and translation of mRNA, increasing transcellular Na+ reabsorption and K+ secretion (Na/K ATPase, Na+ and K+ channels, mitochondrial enzymes)
-increased luminal membrane Na conductance depolarizes luminal membrane potential, thus increasing driving force for K+ efflux across luminal membrane

26

regulation of K+ excretion at low dietary K+

1. decreased distal nephron secretion of K+
-decreased plasma [K+] decreases uptake of K+ by basolateral membrane Na/K ATPase
-decreased driving force for K+ secretion across apical membrane
-decreased synthesis and release of aldosterone by adrenal cortex
2. increased distal nephron reabsorption of K+

27

how does alkalosis affect K+ in distal nephron?

increased pH induces shift in K/H exchange, increasing intracellular k+ (H+ out and K+ in)
-increased K+ increases driving force and rate of K+ transport across luminal membrane
-hypokalemic metabolic alkalosis

28

how does acidosis affect K+ in distal nephron?

decreased pH induces decreased intracellular K+ (H+ in, K+ out)
-decreased intracellular K+ decreases driving force and rate of K+ transport across luminal membrane
-kyperkalemic metabolic acidosis

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