potassium balance

Question 1

where is potassium found (food)?

Answer 1

leafy vegetables, most fruit/fruit juice and in potatoes, especially if they are fried or baked

Question 2

is the concentration of potassium high inside cells or outside cells?

Answer 2

inside

Question 3

ways in which we can lose potassium

Answer 3

urine, regulated by the kidneys - can be loss OR retention

stools and sweat - increase loss when there is intense hear/diarrhoea

Question 4

what organ controls the day to day regulation of potassium levels?

Answer 4

kidneys

Question 5

what substances cause potassium to shift into cells?

Answer 5

insulin, adrenaline and aldosterone

Question 6

the way we gain potassium

Answer 6

diet

Question 7

regulation of K+ homeostasis

Answer 7

Acute regulation:
Distribution of K+ through ICF and ECF compartments

Chronic regulation:
Achieved by the kidney adjusting K+ excretion & reabsorption

Question 8

Potassium functions

Answer 8

1. Determines ICF osmolality → cell volume
2. Determines resting membrane potential → very important for normal functioning of excitable cells
   (i. e. repolarisation of myocardial, skeletal muscle & nerve cells)
3. Affects vascular resistance

Question 9

do intracellular concentrations of ions change?

Answer 9

intracellular concentrations of ions don’t change commonly, but the the extracellular concentration can and does change in certain clinical situations

Question 10

where is 90% of body K located?

Answer 10

intracellularly

Question 11

what maintains low Na+ and high K+ levels?

Answer 11

Na+-K+-ATPase pump

Question 12

role of the sodium potassium pump?

Answer 12

uses the energy from hydrolysis of ATP to do following:

establish a net charge across the plasma membrane (salty banana, inside more negative)

the resting potential prepares nerve and muscle cells for the propagation of action potentials leading to nerve impulses and muscle contraction

accumulation of sodium ions outside of the cell draws water out of the cell and thus enables it to maintain osmotic balance (otherwise it would swell and burst from the inward diffusion of water)

Question 13

after a meal what happens?

Answer 13

slight increase in plasma [K+], which is quickly shifted into ICF compartment

shift is mostly under hormonal control (Insulin, Adrenaline, Aldosterone, pH changes)

Question 14

Hyperkalaemia

Hypokalaemia

Answer 14

plasma [K+] > 5.5mM

plasma [K+] < 3.5mM

Question 15

how is a membrane potential formed?

Answer 15

the creation of ionic gradients

-an ionic gradient is the combination of an electrical and a chemical gradient

Question 16

at rest, is the cell membrane more permeable to potassium or sodium?

Answer 16

potassium

Question 17

how does hypokalaemia (low potassium outside the cell) affect the heart?

Answer 17

• makes the resting membrane potential more negative
• causes hyperpolarisation

-this means it will take even longer to reach the threshold than normal – which will delay firing off an AP, changing the rhythm of the heart (ECG changes)

Question 18

how does hyperkalaemia (high potassium outside the cell) affect the heart?

Answer 18

increase the resting potential, making it less negative, so it approaches the threshold more quickly - firing off AP’s too quickly (ECG changes)

Question 19

what is hypokalaemia caused by?

Answer 19

-renal or extra-renal loss of K+ -restricted intake of K+

eg.
- Long-standing use of diuretics w/out KCl compensation

• Hyperaldosteronism/Conn’s Syndrome (increased aldosterone secretion)
• Prolonged vomiting → Na+ loss → increased aldosterone secretion → K+ excretion in kidneys
• Profuse diarrhoea

Question 20

what happens as a result of hypokalaemia?

Answer 20

↓release of adrenaline, aldosterone and insulin

Question 21

what causes hyperkalaemia?

Answer 21

• acute hyperkalaemia can occur normally following prolonged exercise (released from skeletal muscle into ECF)
• insufficient renal excretion
• increased release from damaged body cells eg. during chemotherapy, long-lasting hunger or severe burns
• long-term use of potassium-sparing diuretics

Question 22

when the plasma K+ concentration becomes greater than 7mM what happens?

Answer 22

asystolic cardiac arrest

Question 23

a rise in plasma K+ stimulates what substance?

Answer 23

insulin - enhances uptake of K+ into cell, lowering plasma levels

Question 24

what infusion can be used to help decrease plasma K+ levels?

Answer 24

Insulin/Glucose infusion used to drive K+ back into cells

-glucose is given with it to prevent hypoglycaemia (drop in blood glucose)

Question 25

how do aldosterone and adrenaline affect K+ levels?

Answer 25

stimulate Na+-K+ pump and cellular K+ influx, lowering plasma K+ levels

Question 26

what increases the RISK of hyperkalaemia?

Answer 26

drugs like β-blockers, ACE inhibitors etc. raise serum [K]

Question 27

what increases the RISK of hypokalaemia?

Answer 27

loop diuretics (used to treat heart failure)

Question 28

Na+ and K+ in the glomerulus

Answer 28

Na+ & K+ filtered freely at glomeruli Plasma & GF have same [Na+] & [K+]

Question 29

how much of the Na+ and K+ is reabsorbed in the GFR?

Answer 29

60-70% Fraction that is reabsorbed in PCT is constant, although the absolute amount reabsorbed varies with GFR

Question 30

K+ movement in PCT | look at slide 19 diagram for Na+ movement

Answer 30

in the PCT, K+ reabsorption is passive and paracellular through tight junctions Na+/K+ ATPase pump on the basolateral side - acts to maintain high potassium levels within the kidney cells, so K+ will diffuse down the concentration gradient through channels in the basolateral membrane into the blood

Question 31

Na+/K+ movement in LoH | look at slide 20 diagram

Answer 31

thin ascending limb get Na & Cl diffusing out as move up into the thick ascending limb, active reabsorption/pumping of Na & Cl out of the fluid and water cannot follow, thereby making stuff in the tubule more and more dilute this is done via a Na/2Cl/K symporter on the luminal membrane which is driven by the [Na] gradient from lumen-cell K+ moves into the medullary interstitial fluid, contributing to the medullary osmotic gradient

Question 32

over 90% of the K+ that is filtered out of the glomerulus goes where?

Answer 32

reabsorbed in PCT and LoH

Question 33

which specific parts of the nephron are in control of the day to day variations of K+ excretion?

Answer 33

the principle cells of the late DCT and collecting duct

Question 34

excretion of K+ --> how it works (slide 21 diagram)

Answer 34

So if we have excess K and want to excrete it out, K+ enters the secreting cells from the blood via the Na-K-ATPase pump. It then diffuses from the cell down the electrochemical gradient through K channels that exist in the luminal/apical membrane into the tubular fluid. The electrical gradient across the luminal membrane normally opposes the exit of K+ from the cell but that gradient is reduced by the Na flux through the EnaC channel in that membrane which is stimulated by aldosterone This is mainly why K+ secretion is coupled with Na+ reabsorption, i.e., the more Na+ reabsorbed by the principle cell, the more K+ secreted A K-Cl cotransporter (symporter) also exists in the apical membrane and transport both K and Cl from the cell into the lumen

Question 35

EnaC channels can be...

Answer 35

inhibited

Question 36

what determines the secretion of K+ into the DCT?

Answer 36

K+ intake Changes in pH -alkalosis will cause more secretion of K+/decrease in [serum K+], and acute acidosis will decrease secretion of pH as you want to retain more in the blood

Question 37

what 3 things help cause a switch between K+ secretion and reabsorption?

Answer 37

1) activity of Na-K-ATPase pump 2) (altering the) electrochemical gradient 3) (altering the) permeability of luminal membrane channel

Question 38

Aldosterone and K+ secretion

Answer 38

aldosterone increases the activity of the Na+/K+ pump, increasing K+ influx into the tubular lumen this contributes to the cell - lumen concentration gradient aldosterone also increases the activity of the ENaC channels, so Na+ reabsorption increases, and the permeability of luminal membrane to K+ increases

Question 39

how does increased plasma [K+] increase K+ secretion? (3 ways)

Answer 39

slows exit from basolateral membrane which increases the intracellular concentration of calcium increased activity of the Na+/K+ pump which increases [K+] within the cell aldosterone secretion is stimulated

Question 40

alkalosis causes what?

Answer 40

an increase in the activity of the Na+/K+ pump

Question 41

how does acidosis limit K+ excretion?

Answer 41

the increase in [H+] of ECF reduces activity of Na/K ATPase pump – this decreases intracellular [K+] so less is excreted

Question 42

how does an increase in tubule fluid flow rate come about?

Answer 42

- ↑GFR - Inhibition of re-absorption - K-wasting diuretics sweeps away secreted K

Question 43

how does ADH affect potassium excretion?

Answer 43

stimulates K secretion

Question 44

when there is severe hypokalaemia which cells become activated?

Answer 44

α-Intercalated Cells of late DCT/CD, which act to reabsorb K+ Potassium hydrogen ATPase pump that gets activated under this situation

Question 45

A fall in ECFV leads to increased Na & fluid reabsorption in PCT, which should cause K secretion into urine to decrease, but it doesn't - why not? slide 30

Answer 45

because, the reduction in ECFV stimulates aldosterone release which stimulates distal potassium secretion as a result of K excretion remains relatively constant

Question 46

what happens when someone is losing a lot of Na+, eg. when vomiting?

Answer 46

the change in Na+ will be picked up as a change in osmolality and detected by the macula densa, which interacts with the JGA and results in renin being released Angiotensin II stimulates the adrenal cortex to release aldosterone – causes increase in sodium retention and increase in water this reabsorption which restores BP, volume and sodium however, we could then be in a situation where we are losing a lot of potassium, so to counteract that if potassium levels get too low we can activate intercalated cells to increase K+ retention.

Question 47

Addison’s Disease | primary adrenal insufficiency

Answer 47

rare disease, adrenal glands produce insufficient steroid hormones damage to cortex, leads to decreased hormone production (sex hormones, cortisol, aldosterone) leads to numerous symptoms eg. deficiency in aldosterone means the body is secreting large amounts of Na, so low serum Na levels, body retaining K - hyperkalaemia Treatment - corticosteroid replacement therapy for life

Question 48

secondary adrenal insufficiency

Answer 48

much more common than Addisons disease the pituitary gland fails to produce enough adrenocorticotropin (ACTH) - hormone that stimulates the adrenal glands to produce cortisol low ACTH output = drop in cortisol production adrenal glands shrink due to lack of ACTH stimulation

Question 49

what is the primary cause of hyperaldosteronism?

Answer 49

Conns Syndrome

Question 50

what happens in Conns syndrome?

Answer 50

excess release of aldosterone - released in the absence of stimulation by Angiotensin II aldosterone stimulates kidneys to increase Na+ reabsorption and K+ excretion - causing hypertension increase in fluid volume causing hypokalaemia, hypernatremia and alkalosis