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sem 2 renal > potassium balance > Flashcards

potassium balance Flashcards

1
Q

where is potassium found (food)?

A

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

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2
Q

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

A

inside

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3
Q

ways in which we can lose potassium

A

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

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

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4
Q

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

A

kidneys

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5
Q

what substances cause potassium to shift into cells?

A

insulin, adrenaline and aldosterone

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6
Q

the way we gain potassium

A

diet

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7
Q

regulation of K+ homeostasis

A

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

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

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8
Q

Potassium functions

A
  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
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9
Q

do intracellular concentrations of ions change?

A

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

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10
Q

where is 90% of body K located?

A

intracellularly

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11
Q

what maintains low Na+ and high K+ levels?

A

Na+-K+-ATPase pump

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12
Q

role of the sodium potassium pump?

A

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)

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13
Q

after a meal what happens?

A

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

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

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14
Q

Hyperkalaemia

Hypokalaemia

A

plasma [K+] > 5.5mM

plasma [K+] < 3.5mM

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15
Q

how is a membrane potential formed?

A

the creation of ionic gradients

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

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16
Q

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

A

potassium

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17
Q

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

A
  • 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)

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18
Q

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

A

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

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19
Q

what is hypokalaemia caused by?

A

-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
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20
Q

what happens as a result of hypokalaemia?

A

↓release of adrenaline, aldosterone and insulin

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21
Q

what causes hyperkalaemia?

A
  • 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
22
Q

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

A

asystolic cardiac arrest

23
Q

a rise in plasma K+ stimulates what substance?

A

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

24
Q

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

A

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

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

25
Q

how do aldosterone and adrenaline affect K+ levels?

A

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

26
Q

what increases the RISK of hyperkalaemia?

A

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

27
Q

what increases the RISK of hypokalaemia?

A

loop diuretics (used to treat heart failure)

28
Q

Na+ and K+ in the glomerulus

A

Na+ & K+ filtered freely at glomeruli

Plasma & GF have same [Na+] & [K+]

29
Q

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

A

60-70%

Fraction that is reabsorbed in PCT is constant, although the absolute amount reabsorbed varies with GFR

30
Q

K+ movement in PCT

look at slide 19 diagram for Na+ movement

A

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

31
Q

Na+/K+ movement in LoH

look at slide 20 diagram

A

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

32
Q

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

A

reabsorbed in PCT and LoH

33
Q

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

A

the principle cells of the late DCT and collecting duct

34
Q

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

A

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

35
Q

EnaC channels can be…

A

inhibited

36
Q

what determines the secretion of K+ into the DCT?

A

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

37
Q

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

A

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

38
Q

Aldosterone and K+ secretion

A

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

39
Q

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

A

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

40
Q

alkalosis causes what?

A

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

41
Q

how does acidosis limit K+ excretion?

A

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

42
Q

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

A
  • ↑GFR
  • Inhibition of re-absorption
  • K-wasting diuretics

sweeps away secreted K

43
Q

how does ADH affect potassium excretion?

A

stimulates K secretion

44
Q

when there is severe hypokalaemia which cells become activated?

A

α-Intercalated Cells of late DCT/CD, which act to reabsorb K+

Potassium hydrogen ATPase pump that gets activated under this situation

45
Q

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

A

because, the reduction in ECFV stimulates aldosterone release which stimulates distal potassium secretion

as a result of K excretion remains relatively constant

46
Q

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

A

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.

47
Q

Addison’s Disease

primary adrenal insufficiency

A

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

48
Q

secondary adrenal insufficiency

A

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

49
Q

what is the primary cause of hyperaldosteronism?

A

Conns Syndrome

50
Q

what happens in Conns syndrome?

A

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

sem 2 renal (10 decks)

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