Renal regulation of ECF potassium Flashcards

1
Q

3 rules for potassium regulation

A

1) all filtered K+ is obligatorily reabsorbed so regulated K+ secretion in fine tuning segments determines K+ excretion and ECF potassium balance
2) variable secretion of K+ accounts for homeostasis

E = F - R + S

E = S because what is filtered is reabsorbed (prox tubule and loop)

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2
Q

bulk of filtered K+ (80%) reabsorbed in __

reabsorption of K+ is ___ and ___ driven by the ___

because it is freely permeable in tight junctions, it is swept along with ___ movement to the ___ side of the epithelium

A

1) proximal tubule
2) paracellular and passive; driven by the bulk flow of water through the tight junctions
3) water movement to the serosal side of epithelium

drives Na+ into serosal, Cl- follows and water follows through tight junction that sweeps along K+

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3
Q

1) in the loop of henle, K+ movement is largely ___, first using the ___ cotransporter at the apical membrane to gain access in a ___ transport process
2) K+ runs down its ____ through a ___ to the serosal/basolateral side
3) loop of henle accounts for ___ % of filtered load reabsorption

A

1) transcellular using Na/K/2Cl; gain access in secondary active transport process
2) electrochemical gradient through a K+ channel
3) 10-15%

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4
Q

secretion of K+ occurs in the ___ of the fine tuning segments (distal tubule/collecting duct)

A

principal cells (single cilia)

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5
Q

Secretory process has two parts

opposite of ___ transport

A

1) basolateral entry of K+ into cell via Na/K atpase
2) apical secretion of K+ into the tubular lumen

coupled to Na+ transport (in aldosterone sensitive cells)

______

reverse Na+ transport

balanced by charge neutrality from Na+ movement in opposite direction

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6
Q

2 steps in secretion

A

1) Na/K atpase to pump K across basolateral membrane into cell (Na out, K in)
2) K+ ion flow passively along electrochem gradient through K+ channel in apical membrane into lumen
3) excreted in urine

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7
Q

Feedback mechanism of incr K+ ingestion

mass action route

A

1) incr K+ ingestion
2) incr K+ in ECF
3) incr basolateral pumping of K+ into cell (MASS ACTION)
4) incr intracellular K+
5) incr driving force for apical K+ movement into lumen (urine)
6) incr K+ secretion and excretion

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8
Q

feedback mechanism of incr K+ ingestion

hormonal route (aldosterone in adrenal cortex)

A

1) incr K+ ingestion into ECF
2) incr stim of adrenal cortex cells
3) incr aldosterone syntehsis
4) incr # Na/K atpase in basolateral and incr in apical Na+ and K+ channels
5) incr basolateral pumping of K+ into cell and MASS ACTION ROUTE

incr permeability of lumenal membrane to K+

6) incr K+ secretion and excretion

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9
Q

What is the flow effect on K+ movement

A

drives passive movement of K+ through potassium channels from cell to lumen (incr permeability of lumenal membrane and incr driving force into lumen)

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10
Q

if you have slow tubular flow, how does that affect movement of K+

A

movement of K+ into lumen is slowed

more time for K+ to build up in tubular fluid before washed away by flow downstream

as lumenal K+ builds up, electrochem gradient for secretion decr (because close to electromchem equilibrium for K+)

secretion decr

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11
Q

if you have incr tubular flow what happens to K+ mvoement

A

K+ will better wash away newly secreted K+ before it builds up

keeps electrochem gradient high

K+ secreted is washed away by fast tubular flow so secretion rate remains elevated

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12
Q

what happens with loop diuretic on tubular flow

A

1) block Na/K/2Cl
2) inhibit NaCl excretion, inhibit H2O reabsorption
3) incr tubular flow because more H2O stays in tubule
4) incr K+ secretion and incr K+ excretion –> K+ wasting

also diuretic incr K+ excretion to 150% rate (10x faster rate of excretion than just inhib Na/K/2Cl due to incr tubular flow)

2) 25% NaCl in asecending limb drives out water from descending limb and distal tubule/collecting duct (ADH area) keeping interstitium hypertonic

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13
Q

How does K+ movement change if you applied lasix

A

block Na/2Cl/K transporter in descending limb of loop of henle

decr hypertonicity of interstitim (less Na/K/Cl move out)

less water reabosrbed

incr tubular flow

incr K+ excretion

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14
Q

how does alkalsosis affect K+ level and secretion

A

alkalosis –> hypokalemia

1) incr ECF pH (decr [H+]; as H+ leave, induce K+ to enter

loss of H+ from cells due to lower driving force for H+ into cells –> (H+ normally block Na+ channel) –> incr K+ permeability of apical K+ channels for K+ excretion

2) shift K+ from ECF into all cells
3) incr driving force for apical secretion and excretion

incr passive entry of K+ into principal cells

incr gradient for K+ excretion in Step 2 (across lumen) –> incr K+ excretion (hypokalemia)

4) decr K+ in ECF (hypokalemia)
5) also incr permeability of K+ in distal tubule and collecting duct on apical, incr K+ secretion

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15
Q

how does incr ECF pH affect K+ level

A

1) shift of K+ into cells
2) decr K+ concentration of ECF –> hypokalemia

incr K+ channel permeability because less H+ inhib apical K+ channels –> incr K+ secretion

3) incr intracellular K+
4) incr driving force for apical K+ secretion into lumen (incr permeability)
5) incr K+ secretion and excretion beyond needed for ECF balance–> hypokalemia

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16
Q

what does mass action mean

what is the impact of mass action on K+ regulation

A

Mass action = passive process driven by chemical kinetics

only good for K+ excess –> good for large change but as K+ return to normal, delay when chemical process slows

17
Q

does hypokalemia cause alkalosis?

A

1) give patient loop diuretic
2) patient becomes hypokalemic
3) also become alkalotic

18
Q

Normal filtration K+ per day

Normal excretion K+ per day

A

30 g K+ filtered

0-45 g K+ excreted

19
Q

Reabsorption occurs where?

all of filtered potassium is obligatory reabsorbed, hence potassium secretion in fine tuning segments determines K+ excretion and ECF K+ balance

A

via principal cells of distal tubule/collecting duct

20
Q

K+ is a ___ for Na+/K+ ATPase

A

required cofactor

binding of K+ to pump is rate limiting step in exchange pump

more K+ in serosa more quickly pumped into cell

21
Q

Mass action effect is most effective when?

If you have lower K+, what problem

A

slows down

problem with membrane excitability –> cardiac arrhythmias

22
Q

Effect of aldosterone on K+ (3)

A

1) incr Na/K atpase
2) incr Na+ entry on apical to incr K+ entry into cell
3) incr K+ on apical to allow for more passive diffusion

23
Q
A
24
Q

Effect of primary hyperaldosteronism on tubular flow

A

aldosterone= incr K+ secretion and incr Na reabsorption, thereby decr tubular flow

25
Q

Primary vs. Secondary hyperaldosteronism

A

Primary = incr K+ secretion because incr ECF volume, incr MAP, incr filtration (tubular flow normal or incr)

Secondary = cardiac insufficiency, decr MAP, (still incr aldosterone due to RAAS), decr K+ secretion becasue decr GFR, decr filtration flow, decr tubular flow

26
Q

alkalosis incr ___, tends to produce ___

A

incr K+ secretion, hypokalemia

27
Q

Effect of low acidosis (mild acidosis) on K+ levels

Effect of severe acidosis on K+ levels

A

1) shift K+ from cells to ECF
2) apical K+ channels inhib by incr H+
3) decr K+ secretion

____

inhibited Na reabsorption and inhib water reabs

incr tubular flow, incr K+ secretion, hypokalemia