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HMS Homeostasis II > Potassium Homeostasis > Flashcards

Potassium Homeostasis Flashcards

1
Q

In hypokalemia, how does the kidney adapt in order to avoid further potassium losses?

A
  • Stimulation of ammoniagenesis to trap more protons, favoring loss of H+ over K+ in the distal nephron
  • Angiotensin II decreases distal sodium delivery, preventing K+ loss by limiting the ENaC loop
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2
Q

In hyperkalemia, how does the kidney adapt in order to facilitate potassium excretion?

A
  • Aldosterone is activated independent of angiotensin II to promote activity of ENaC, the negative luminal charge and potassium secretion, while maintaining distal sodium delivery
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3
Q

Signs and symptoms of hyperkalemia

A
  • Increased resting potential of neurons
    • This will affect the inward Na+ current and Vmax of the action potential.
    • When the resting membrane potential is less negative, this will slow the influx of Na+
    • Prolonged membrane depolarization, and thereby QRS interval
  • On ECG:
    • Loss of p waves
    • “peaked T waves”
    • Prolonged/widened QRS
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4
Q

. The kidney is superb at potassium excretion, but . . .

A

. The kidney is superb at potassium excretion, but needs time to do so.

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5
Q

Kayexalate

A
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6
Q

Change in depoarization in hyperkalemia

A
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7
Q

Cell death in potassium regulation

A

Cell death can result in release of potassium (and phosphate) into the circulation.

The most common is severe damage to muscles (Rhabdomyolysis) and destruction of cancer cells (tumor lysis). The latter can be spontaneous (rare-this occurs when the tumor outgrows its blood supply) or related to chemotherapy.

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8
Q

Lab test errors for potassium

A

Hypokalemia is almost never an error, however a reading of hyperkalemia may be “pseudohyperkalemia”

“pseudohyperkalemia” is a laboratory artifact that occurs when the cells lyse in the test tube and the laboratory reports a high potassium value, but the patient’s potassium is normal

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9
Q

Calcium gluconate

A

Given in the case of hyperkalemia to stabilize heart membranes. Quite effective in doing so, changes will be readily visualized on ECG.

Calcium is the real active agent here, but know, calcium chloride can actually be quite toxic. It is only given via venous access and calcium gluconate should be given over calcium chloride whenever possible.

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10
Q

Why are patients on thiazide diuretics so at risk for a metabolic alkalosis?

A
  1. High distal salt delivery encourages loss of H+
  2. Mild volume depletion induced by thiazides activates RAAS, inducing proximal HCO3- reabsorption, maintaining the alkalosis

Note that this is only the case when a volume depletion is induced, so giving to patients with volume overload and low RAAS activity is fine.

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11
Q

Excretion of potassium in the healthy distal nephron depends on two factors:

A
  1. Distal delivery of sodium (this is affected by angiotensin II activity!)
  2. The action of aldosterone
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12
Q

The normal serum potassium is very tightly regulated within a narrow range of ____. The restriction of potassium to the intracellular space is maintained by the ___.

A

The normal serum potassium is very tightly regulated within a narrow range of 3.4 to 5.2 mEq/L. The restriction of potassium to the intracellular space is maintained by the Na+- K+- ATPase.

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13
Q

Angiotensin II and potassium

A
  • Decreases distal Na+ delivery, which thereby decreases K+ secretion
  • Directly inhibits ROMK, to the same effect, but more directly distal
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14
Q

Potassium in diabetic ketoacidosis

A

In diabetic ketoacidosis, K+ is lost in the urine with the negatively charged ketones but the plasma K+ may be high because of lack of insulin

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15
Q

Causes of hyperkalemia

A
  • EXCESSIVE INTAKE- since the kidney is excellent at excretion, there is also usually renal dysfunction
  • CELLULAR REDISTRIBUTION
    • Inadequate shift into cells because of insulin deficiency, nonselective beta blockade
    • Cell destruction
    • Hyperosmolar state, water drawn from cells, increased intracellular potassium, leak from cells
    • Acidemia (usually minor effect)
  • DECREASED EXCRETION
    • ​Decreased “distal delivery” ** most important
    • Insufficient aldosterone, mineralocorticoid receptor blocking, or defect in mineralocorticoid signaling
    • Too few nephrons (chronic kidney disease)
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16
Q

Signs and symptoms of hypokalemia

A
  • May be asymptomatic
  • Muscle cramps
  • Weakness
  • Arrhythmia
  • U waves on ECG representing delayed ventricular repolarization
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17
Q

Adverse effects of loop diuretics

A
  • Volume depletion
  • Hypokalemia
  • Ototoxicity (the same Na/K/2Cl transporter is found in the Organ of Coti)
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18
Q

Potassium in the collecting duct

A

In the collecitng duct, distal delivery of Na+ and the presence of aldosterone facilitate K+ secretion via ENaC and ROMK/Maxi-K.

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19
Q

pH in potassium regulation

A

In acidemia, intracellular potassium tends to be lost to the ECF in exchange for protons (intracellular K+ down)

In alkalemia, potassium tends to bleed into cells in exchange for protons (intracellular K+ up).

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20
Q

In the setting of hyperkalemia, how can potassium be forced to “shift into cells” in order to allow more time for other therapeutic interventions which will favor removal from the body?

A

By giving insulin or dextrose (which will then result in endogenous insulin release)

Another strategy is to give a beta-agonist such as albuterol nebulizer.

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21
Q

As the filtrate flows down the proximal tubule, the luminal voltage shifts from. . .

A

As the filtrate flows down the proximal tubule, the luminal voltage shifts from slightly negative in the early part of the proximal tubule to slightly positive at the most distal aspect of the proximal tubules.

This shift in transepithelial voltage provides an additional driving force that favors K+ movement through the low-resistance paracellular pathway

22
Q

Plasma osmolality in potassium regulation

A

Increased plasma osmolality will lead to movement of water from cells. This will lead to a transient increase intracellular [K+] concentration and then lead to outward diffusion of K+

23
Q

Patient presents with severe flank pain radiating to the back, along with hematuria. A urine specimen is examined under the microscope and is pictured below. What is the diagnosis?

A

These are calcium oxalate crystals, with a characteristic [X] pr ‘envelope’ morphology. The diagnosis is hypercalciuria-induced nephrolithiasis and recommended treatment includes sonic kidney stone ablation along with thiazide diuretics.

Unfortunately, thiazides here may also lead to hypercalcemia, so careful dosing and management is required.

24
Q

Important side effects of ACE inhibitors

A
  • Angioedema (if this happens, patient cannot take any more ACE inhibitors of any type)
  • Dry cough
  • Decreased GFR
  • Teratogenesis (contraindicated in all pregnant women and women who are intend to become pregnant)
25
Q

Thiazide’s effect on calcium

A

Blocking the NCC actually encourages transport of calcium through the adjacent Ca2+ ion channel in the distal convoluted tubule, facilitating reabsorption of calcium.

For this reason, they are useful for hypercalciuria. This is a condition in which elevated urine calcium results in the formation of calcium oxalate crystals which are a form of kidney stone, causing nephrolithiasis.

26
Q

Patiromer

A
27
Q

Any agent that interferes with the RAAS system may. . .

A

. . . lead to downstream hyperkalemia, mostly due to aldosterone

28
Q

Spironolactone and eplerone

A
  • K+ sparing diuretics
  • Mineralocorticoid receptor blockers
  • fewer ENaC are deployed to the luminal membrane and there is less Na+ reabsorption
  • the lumen will be less negative and there will be less K+ lost (and less H+ lost from the neighboring cell).
29
Q

Under normal circumstances, this results in a resting membrane potential of about ___

A

Under normal circumstances, this results in a resting membrane potential of about -90 mV (cell interior is negative).

This negative potential difference sets the stage for the action potential in excitable cells like muscle and nerves.

30
Q

The potassium [K+] inside cells is approximately ___ whereas the potassium concentration outside cells, in the extracellular space, is just ___

A

The potassium [K+] inside cells is approximately 140 mEq/L whereas the potassium concentration outside cells, in the extracellular space, is just 4.0 mEq/L

31
Q

Thiazide diuretics in potassium regulation

A

Thiazide diuretics block the activity of the NCC in the distal tubule. Blockade of NCC will lead to an increase in distal delivery of Na+ and Cl- and this will favor collecting duct losses.

32
Q

In the kidney, potassium in the initial filtrate is . . .

A

In the kidney, potassium in the initial filtrate is nearly entirely absorbed in the proximal tubules and then secreted in the distal nephron by the principal cells

33
Q

Treatment of hypokalemia

A
  • Replete losses
    • Losses may be considerable. Indeed, once the serum K+ is at 2 mEq/L, this may represent several 100 mEq defecit.
    • Large doses of potassium may be given to replete defecits orally
    • Intravenous doses are given only cautiously and in small doses
  • Limit further losses
    • ​diuretic management
    • treatment of underlying disease
34
Q

Acetazolamide in potassium regulation

A

Acetazolamide is a carbonic anhydrase inhibitor. It increases urine pH, may cause acidosis, and acts as a diuretic by decreasing bicarbonate reabsorption. Potassium comes along for the ride, and this may cause hypokalemia, and sodium may also be lost.

35
Q

Potassium in the distal convoluted tubule

A

The DCT does not have important K+ channels and does not play a direct role in potassium homeostasis,

HOWEVER, blockade of the NCC by thiazide diuretics can have an important effect on potassium because of the increase in distal delivery of Na+ to the distal nephron. This causes potassium loss.

36
Q

Catecholamines in potassium regulation

A

During exercise, K+ is released from cells.

Catecholamines stimulate the Na+ K+ ATPase and help return K+ to the cells.

37
Q

Potassium in the loop of Henle

A

The filtrate that arrives in the loop of Henle has almost no potassium. Yet the major transporter in this region, the electroneutral Na+ K+ 2Cl- co transporter (NKCC) requires each position of the transporter to be filled in order for transport

This is where ROMK comes in. Potassium diffuses through ROMK and then helps drive the NKCC reabsorption of sodium and chloride.

38
Q

Causes of hypokalemia

A
  • INADEQUATE INTAKE- since potassium is in every type of diet, this is unusual unless there are also losses
  • SHIFT INTO CELLS - because of insulin, beta adrenergic stimulation, increased extracellular pH (pH has only small effect)
  • EXTRARENAL LOSS - LOWER GI tract (primarily diarrhea, very little potassium in vomit) or excessive losses from skin (sweat, burns)
  • RENAL LOSS
39
Q

Insulin in potassium regulation

A

After a meal, insulin is released into the blood in response to glucose.

Insulin promotes entry of K+ into hepatic and skeletal muscle cells by increasing the activity of the Na+ K+ ATPase.

40
Q

Patient presents with significant edema due to fluid overload with a metabolic alkalosis. What is the diuretic of choice?

A

Acetazolamide

The effects of acetazolamide will result in both diuresis and reduced bicarbonate retention, combating the alkalosis.

41
Q

Amiloride and triamterene

A
  • K+-sparing diuretics
  • Block ENaC
  • This means that the lumen will be less negative and there will be less K+ lost (and less H+ lost from the neighboring intercalated cell).
42
Q

Furosemide in potassium regulation

A

Loop diuretics block the activity of NKCC. Mimics Bartter’s syndrome, a deficiency of NKCC.

Potassium lost through ROMK is not reclaimed by NKCC, and is instead just excreted and lost. The accompanying Na+ and Cl- are also not absorbed here.

Thus, distal salt delivery is increased. This also causes secretion of K+ at the collecting duct.

43
Q

ECG in Hypokalemia

A
44
Q

Lokelma

A
45
Q

Unusual potential side effect of mineralocorticoid receptor antagonists

A

Some men develop gynecomastia. This is an important effect do tell your male patients about since it is potentially very distressing and they are unlikely to bring it up since most people do not readily see the correlation.

46
Q

Treatment of severe hyperkalemia

A
47
Q

ECG appearance in hyperkalemia

A
48
Q

Where does the trade name Lasyx (for furosemide) come from?

A

Lasts-six

For lasts six hours!

The half-life of furosemide is 90 minutes, so by 6 hours all of it has been cleared following a bolus dose.

49
Q

If there is a large number of anions in the proximal tubule, . . .

A

If there is a large number of anions in the proximal tubule, this will limit the reabsorption of potassium

Examples of this include failure of bicarbonate reabsorption, ketoacids, and certain medications like penicillin. All of these are documented to increase potassium losses in the proximal tubule.

50
Q

Treating hyperkalemia

A

For shifting potassium into cells, insulin, dextrose, or a beta-agonist like albuterol may be utilized.

51
Q

What types of things might result in a falsely high lab measurement of potassium? (pseudohypokalemia)

A

HMS Homeostasis II (35 decks)

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