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Renal Week 1 > Potassium Metabolism > Flashcards

Potassium Metabolism Flashcards

1
Q

What compartment contains the majority of K+?

A

Our body approximately has 3000-4000 meq of K. 98% of the K is intracellular, intracellular storage contain about 3300 meq of K.

Rest of the K about 2% is in the extracellular fluid (65 mEq)

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2
Q

What is the intracellular conc of K+ normally?

A

about 150 meq/L

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3
Q

What is the extracellular conc of K+ normally?

A

about 4.5 meq/L

NOTE: when we check K+ in the body, it is the extracellular K+ we are checking

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4
Q

What organs contain the most K+?

A
  • muscle (2500 mEq)
  • liver (250 mEq)
  • RBC (250 mEq)
  • Bone (300 mEq)

so damage to these will release large amounts of K+

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5
Q

How much K+ is consumed in a normal diet? How is it excreted or is it retained?

A

~100 meq of K.

If the kidney is functioning normally, about 90-95% of that is excreted through the kidney.

NOTE: A minimal amount of K is excreted through large bowel in the stool.

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6
Q

What is the result of most of K+ being intracellular?

A

Cellular damage will release large amount of K into the ECF. K conc in the extracellular fluid or blood can be changed by movement of small amount of K out of the large K storage in ICF or impairment of renal excretion of K.

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7
Q

Note on internal vs. external K+ balance.

A

External balance involves K intake with diet and K excretion through kidney and GI tract.

Internal balance of K is maintained by regulation of K distribution between intracellualr and extracellular compartments.

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8
Q

Where is the majority of K+ reabsorbed?

A

PCT (65%)
Thin ascending limb (25%)

A small amount K is reabsorbed in the cortical and ssOUTER medullary collecting duct by the intercalated cells – but the amount is very small, and it usually only becomes significant in case of hypokalemia

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9
Q

T or F. K that is secreted in urine mostly comes from K secretion from the principal cells in the collecting tubules in the cortex and in the outer medulla and also inner medullary collecting duct.

A

T.

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10
Q

How is K+ absorbed in the TALH?

A

with the Na/K/2Cl transporter located in the luminal border

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11
Q

What happens to the Na+ and Cl- that is absorbed?

A

Na+: returned to the systemic circulation by the NaK ATPase in the basolateral membrane

Cl-: The Cl is returned by a selective Cl channels in the basolateral membrane

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12
Q

What happens to the K+ that is absorbed?

A

Some of the K that is reabsorbed is recycled back across the luminal membrane by a selective K channel (ROMK).

ROMK (renal outer medullary potassium channel)

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13
Q

What does the K+ transport back into the tubular lumen allow for?

A

1) continued function of the Na/K/2Cl transporter
2) The K that comes out increases the lumen positivity and allows for passive paracellular transport of +ve charges such as K, Ca, Na, and Mg. to the ISF

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14
Q

What does the drug Furosemide do?

A

inhibiting the NaK2Cl transporter (as does Bartter’s syndrome)

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15
Q

Where is K+ secreted?

A

In principle cells of the Collecting duct (cortical and medullary)

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16
Q

How does K+ secretion occur?

A

The K secretion is associated with Na reabsorption in the segment.

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17
Q

How does Aldosterone affect K+ secretion in the principle cells of the CD?

A

Aldosterone after entering the cells combine with the specific aldosterone receptor in the cytosol.

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18
Q

What does the aldosterone receptor do once bound?

A

The hormone receptor complex migrates to the nulceus where it forms new protein including Na and K channels for the apical membrane, and

The positive effect of aldosterone on the NaK ATPase pump moves 3Na out of the cells and 2K into cells

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19
Q

What does the movement of the NaK ATPase pump allow for?

A

The movement of Na outside the cells promotes passive diffusion of luminal Na into the cells.

NOTE: Aldosterone promotes this passive diffusion by formation of newer Na channel

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20
Q

What does movement of Na+ into the cell allow for?

A

Movement of the positively charged Na creates relative electronegativity in the lumen. To maintain the electroneutrality in the lumen K is passively secreted out of the cells into the tubular lumen mainly and Cl gets reabsorbed through the paracellular pathway to the ISF.

NOTE: Aldosterone stimulates the synthesis and formation of K channel in the apical membrane.

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21
Q

What things affect the amount of K+ secreted in the CD?

A
  1. concentration gradient of K across the basolateral membrane – it depends upon serum K concentration
  2. The electrical gradient across the luminal membrane – it depends upon the reabsorption of Na through the Na channels in the luminal membrane. Which in turn depends upon the Na concentration in the tubular lumen via distal delivery of Na
  3. K+ permeability of the luminal membrane
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22
Q

What is the effect of less Na being reabsorbed in the PCT or LOH?

A

More Na+ will be delivered to the collecting tubule which will cause more Na reabsorption by the ENa channel and more K secretion (loss in urine)

On the other hand if we do not have enough distal Na delivery, it will impair K secretion in collecting tubule.

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23
Q

What is K+ permeability of the luminal membrane in the CD affected by?

A

that depends upon the number of open K channel on the luminal membrane. Which is affected by the aldosterone.

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24
Q

So what is the effect of hyperaldosteronism on K+?

A

increase K+ secretion and lead to low serum K or hypokalemia.

On the other hand if Aldosterone level is low which is known as Hypoladosteronism will decrease K+ secretion and elevated serum k or hyperkalemia.

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25
Q

How does increased distal tubular flow of Na affect distal K+ secretion?

A

On a control diet as the distal tubular flow increases distal K secretion also increases.

This happens in presence of aldosterone. High K diet will enhance the effect of the distal tubular flow. The enhnaced K secretion associated with higher K diet can be explained by the other 2 factors that mentioned in the previous slide. High K diet will increase the serum K level which will increase the 1. K concentration gradient and as well as 2. serum aldosterone level. As a result distal K secretion is increased.

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26
Q

On the other hand low K diet will reduce the distal K secretion. Why?

A

Even with increasing the distal tubular Na delivery K secretion will not increase, this happens because low K will remove stimulation of aldosterone secretion.

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27
Q

What things can decrease K+ secretion?

A
  • renal failure.
  • decreased distal tubular flow (dysfunctional CD) or delivery of Na+
  • hypoaldosteronism (will lead to hyperkalemia)
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28
Q

What things can increase K+ secretion?

A
  • increased distal Na+ delivery (loop diuretics, thiazides, Bartter’s and Gitelman’s)-impair proximal Na absorption
  • hyperaldosteronism (secondary or primary)
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29
Q

How is internal K balance maintained?

A

by regulating the K transport across the cell membrane via a Na-K-ATPase pump that maintains high intracellular K+ levels

NOTE: Because of the high gradient some K+ comes out of the cells by passive transport through the K channel.

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30
Q

There are several factors that promotes the K movement across the cell membrane. Name some.

A
  • Plasma K concentration
  • Insulin
  • Epinephrine
31
Q

What does insulin do?

A

Insulin moves K inside the cells by stimulating a NaH exchanger on the cell membrane that moves Na inside the cell in exchange for H, this intracellular Na than activate the NaKATPase pump and moves K inside the cells.

32
Q

What does epi do?

A

activates the NaKATPase pump by stimulating beta2 receptors (Any other hormones or drugs, such as albuterol, that can stimulate beta receptor will stimulate NaKATPase pump.)

33
Q

What is the effect of diabetes or a BB on intracellular K+?

A

the activity of the NKATPase pump will be impaired, with decrease movement of K from ECF to ICF. But the K channel which is not affected by the hormones will remain open and will continue to move K ICF to ECF which will result in elevated K in ECF

34
Q

How do acid-base disturbances affect internal K+ balance?

A

extracellular acidosis promotes H+ movement inside the cell and K+ out and vice-versa with alkalosis

35
Q

T or F. Metabolic acid-base disturbances have a greater effect than respiratory disturbances.

A

T. Metabolic acidosis due to organic acids (ketoacidosis, lactic acidosis) have smaller effects than do acidosis due to mineral acids.

36
Q

How does plasma tonicity or osmolality affect serum K+?

A

Elevated plasma osmolality or hypertonicity can happen in hypernatremia or hyperglycemia.

Hypertonic ECF will cause movement of ICF water to ECF. When water moves out of cell, it drags K out along with it as the intracellular to extracellular conc gradient increases– which is known as solvent drag.

37
Q

What are some situations that might lead to increases plasma tonicity due to hyperglycemia?

A

This happens in diabetic ketoacidosis or diabetic hyperosmolar state, where ECF tonicity is increased due to elevated glucose concentration.

38
Q

What other thing could lead to hyperkalemia?

A

cell lysis. This usually happens when there is Rhabdomyolysis or hemolysis

NOTE: The opposite thing can happen during rapid cellular proliferation such as in case of malignancy: extracelluar K is taken up rapidly by proliferating cells, which lead to fall in ECF K+

39
Q

What is hyperkalemia defined as?

A

serum K above 5.5 in ECF

40
Q

What are the three broad types of hyperkalemia?

A
  • too much K with our diet,
  • K excretion impairment
  • balance between ICF and ECF is altered with release of K from ICF.
41
Q

In patients with normal function it is very unlikely to increase serum K level by po or IV intake. Why?

A

Because normal kidney is very efficient in removing extra K. So hyperkalemia most commonly happens in patients who have some degree of renal failure.

42
Q

What are the EKG manifestations of increased K+?

A

tall, peaked T wave at slightly elevated K+ levels followed by:

  • widening of the QRS complex,
  • prolonged PR inerval,
  • loss of p wave,
  • further widening of QRS complex.

And ultimately sine wave which indicate ventricular tachycardia (at very high conc of K+).

43
Q

What is the main complication of hyperkalemia?

A

cardiac toxicity. It can present as EKG changes that we just discussed, it can also cause defects in cardiac impulse conduction, and arrhythmias.

Similar effect on skeletal and smooth muscle can cause weakness, paralysis.

44
Q

T or F. The arrhythmias that are associated associated with hyperkalemia is Bradyarryhthmias.

A

T. Why?

45
Q

How is hyperkalemia treated?

A
  • IV calcium to stablize cardiac muscle cells if needed (onset in 1-3 minutes and duration is 30-60 min)
  • Lower serum K+ with insulin, B2 agonists, HCO3- to promote cellular uptake
  • Lower serum K+ with diuretics, dialysis, or cation exchange resin (kayexalate) to move K+ outside the body
46
Q

How does kayexalate work?

A

can excrete K+ in stool (onset in 2-3 hrs and acts for about 4-6 hrs)

47
Q

Which drug that promotes increased cellular K+ uptake acts longest? Which has the earliest onset?

A

insulin (onset-30 min; duration 4-6 hrs)

HCO3- (onset-15 min; duration 1-2hrs)

Albuterol (onset-30 min; duration 2-4hrs)

48
Q

Onset and duration of furosemide

A

onset-5 min

duration- 2hrs

49
Q

What is hypokalemia defined as?

A

less than 3.5

50
Q

What are the three broad causes of hypokalemia?

A
  • dietary deficient of K,
  • increased K excretion,
  • if the balance between ICF and ECF is altered with movement of K from ECF to ICF.
51
Q

T or F. Cutaneous loss is rarely a cause for hypokalemia.

A

T.

52
Q

What are normotensive hypokalemic disorders?

A

excessive renal loss of K+ with normal BP

53
Q

Normotensive hypokalemia can be associated with metabolic alkalosis or metabolic acidosis. What are some cause of NH associated with metabolic alkalosis (high HCO3-)??

A

diuretics, vomiting, and Bartter’s and Gitelman’s syndrome

54
Q

What are some cause of NH associated with metabolic acidosis (low HCO3-)?

A
  • renal tubular acidosis, which are a group of disorders where there is dysfunction of renal tubules that cause low serum potassium and acidosis
  • In ureteral diversion surgery, ureters are detached from the urinary bladder and attached to ileum where it is known Uretero-ileostomy or to the sigmoid colon where it is known as uretero-sigmoidostomy. In both cases colon losses HCO3 and reabsorbs NH4Cl.
55
Q

There are 3 different types RTA. Which types are associated with hypokalemia?

A

Type 2 and 1 RTA are associated with hypokalemia.

56
Q

What is the main site for K+ reabsorption?

A

PT

57
Q

Dysfunction in proximal tubule can cause ____ where there is impairment in HCO3 absorption as well as K reabsorption

A

type 2 RTA

58
Q

How do Furosemide and Bartter’s syndrome cause hypokalemia?

A

In TALH diuretics Furosemide and Bartter’s syndrome can cause problem with NaK2Cl co-transporter which will impair Na reabsorption

This will result in increased Na delivery to the CD and increased K loss

Similar thing happens in the distal tubule with diuretics Thiazide and Gitleman’s syndrome which cause problem with Na transporters.

59
Q

What causes RTA type 1?

A

Dysfunction of the collecting duct

60
Q

How does persistent vomiting cause hypokalemia?

A

Vomiting will cause loss of fluid and H and Cl. Loss of fluid and inability to intake will decrease ECF volume, hypotension and release of hormone Aldosterone.

Normally in distal tubule Na and Cl get reabsorbed together that maintain electroneutality of the tubule. So when Cl is lost, there will be less Cl delivered to the distal tubule. Instead Na will be delivered to distal tubule with negatively charged HCO3. At the same time elevated aldosterone in collecting tubule will cause reabsorption of Na which will increase electro negativity of the lumen resulting increased secretion of K and H.

So you can find hypokalemia, metabolic alkalosis in blood but aciduria in urine, that is why the term paradoxical aciduria.

61
Q

Is vomiting associated with metabolic alkalosis or acidosis?

A

Loss of H will result in elevated HCO3 level in blood or metabolic alkalosis.

62
Q

Hypertensive disorders with hypokalemia are usually due to what?

A

increased activity of the aldosterone. It can be due to primary hyperaldosteronism associated with adrenal gland tumor or adrenal hyperplasia, or it can be secondary to elevated renin secretion from renin secretion tumor or renal artery stenosis. In both cases hypokalemia occurred due to stimulation of aldosterone

63
Q

Are there any other causes of hypertensive disorders with hypokalemia?

A

Yes, can be caused by glucocorticoid release

64
Q

What can glucocorticoids do?

A

Glucorticoids can stimulate the aldosterone receptors in the distal tubular cells, although not as strongly as aldosterone (causing a small degree of hypokalemia).

Among them most common that you are going to see is the exogenous steroid, where patient will be receiving high dose oral or IV streroid in the form of prednisone or hydrocortisone. This is common in the setting of Rx for patients with transplantaion, autoimmune disease, obstructive pulmonary disease.

65
Q

Like hyperkalemia, hypokalemia is also characterized by some specific changes in EKG.

A
  • flat T waves
  • U wave formation after t waves
  • ST deprsssion with severe hypokalemia.
66
Q

What symptoms are associated with chronic hypokalemia?

A

Most are asymtomatic. Sx varies with organ systems.

However, its effect is most pronounced on muscles where is K+ is need for neuromuscular transmission (producing weakness and rhabdomyolysis)

67
Q

The arrythmias associated with hypokalemia are _____.

A

tachyarrythmias

68
Q

Other symptoms of chronic hypokalemia?

A
  • elevated BP (HTN).

- ADH resistance and lead to nephrogenic DI.

69
Q

What is the treatment for hypokalemia?

A

K replacement except in very very rare cases where there is massive intracellular shift of K.

K supplement is usually given as KCl or KPO4 if there is concomitant PO4 deficiency.

70
Q

How can you estimate how much K+ is needed?

A

Because K is an intracellular lyte, extracellular K level or serum K level only gives us approximate deficiency of total body K. Usually it is estimated loss of 200 to 400 meq total body K will result in drop of serum K from 4 to 3.

71
Q

How should K+ be infused?

A

IV. K should be given slowly 10 meq over 2 hrs. Rapid infusion of K can cause cardiac arrest.

72
Q

What is another treatment option for hypokalemia?

A

K+ sparing diuretics. This is usually used in cases of chronic hyopokalemia.

73
Q

What are the types of K sparing diuretics?

A

2 different types, both of which work on the collecting tubule and decrease K secretion.

  1. Aldosterone receptor antagonists: Which act by preventing the binding of aldosterone with the aldosterone receptors.
  2. ENa channel inhibitors (amiloride, Triamterene) These act inhibiting the ENa channel Inhibiting this channel will increase the +ve charges in the lumen, which in turn will prevent K secretion.
74
Q

What level of GFR forces patients to maintain a low K+ diet? Why?

A

30 ml/min because the kidney cannot effectively secrete it

Renal Week 1 (20 decks)

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