Chapter 5: Potassium

Question 1

Describe how (what mechanism) the basolateral Na+ ,K+, ATPase pump affects K+ excretion

Answer 1

K+ moves into the cell and Na+ out of the cell –> increases the IC [K+] –> concentration gradient that favors excretion of K+ into the lumen

Question 2

what are the 2 mechanisms by which water reabsorption promotes K+ reabsorption in the proximal tubules

Answer 2

1. solvent drag
2. water diffusion out of lumen –> leaves behind higher cc of solutes –> high luminal [K+] –> lumen positive transepithelial electrical potential difference –> K+ reabsorption

Question 3

How does a lumen negative transepithelial electrical potential difference influence K+ excretion or reabsorption?

Answer 3

lumen negative charge –> attracts positively charged K+ –> more excretion

Question 4

How does a lumen positive transepitheliam electrical potential difference influence K+ excretion or absorption?

Answer 4

Lumen positive charge –> IC is more negative –> K+ favor movement into the cell –> more K+ reabsorption

Question 5

How do loop diuretics affect K+ reabsorption?

Answer 5

affect transcellular Na+, K+, Cl- cotransporter in the ascending loop of Henle –> less Na, K, and Cl reabsorption

Question 6

What hormone stimulates the electrogenic Na channel

Answer 6

Aldosterone

Question 7

How does the electrogenic Na channel enhance K+ excretion?

Answer 7

increases the IC [Na+] –> creates negativity in the tubular lumen –> negativity draws K+ ions out of the cells into the lumen

Question 8

What is the main function of the alpha intercalated cells in the distal nephron?

Answer 8

hydrogen ion secretion and HCO3 reabsorption –> acid secretion and K+ reabsorption

Question 9

What is the main function of the beta intercalated cells in the distal nephron?

Answer 9

bicarb secretion –> base secretion

Question 10

What are the 3 determinants of K+ excretion?

Answer 10

1. chemical concentration gradient of K+ between IC and tubular lumen
2. tubular flow rate
3. transmembrane potential difference across luminal membranes of tubular cells

Question 11

How does increased ingestion/GI absorption of K+ influence K+ secretion in the kidneys

Answer 11

more K+ in ECF for K+, Na+, ATPase pump –> more IC K+ –> concentration gradient favors K+ movement into the tubular lumen

Question 12

What is the most important hormone affecting K+ excretion and how does it affect it?

Answer 12

Aldosterone

• increases number of open electrogenic Na channel –>
  1. electronegativity of the tubular lumen –> promotes K+ secretion into the lumen
  2. increased IC [Na+] –> increased activity of basolateral Na+, K+, ATPase pump –> increased IC [K+] –> increased K+ excretion into the lumen

Question 13

Where will you find a higher potassium concentration, serum or plasma?

Answer 13

Serum, because platelets release potassium during the clotting process.

Question 14

What conditions can cause pseudohyperkalemia?

Answer 14

Thrombocytosis and hemolysis in breeds that have a HK phenotype (Shiba, Akita, Chinese Shar Pei and Jindo breed in Korea).

Question 15

What is the formula for potassium fractional excretion?

Answer 15

FEk = [(UK x SCr)/(UCr x SK)] x 100

Question 16

What are the main causes of hypokalemia?

Answer 16

• Decreased intake
• Translocation (ECF –> ICF)
• Increased loss

Question 17

True or False: Pure potassium depletion leads to metabolic alkalosis in dogs.

Answer 17

False, it leads to metabolic acidosis.

Question 18

Under which potassium concentration can you see frank rhabdomyolysis?

Answer 18

Less than 2 mEq/L.

Question 19

True or False: Hypokalemia delays ventricular repolarization and increases the duration of the action potential.

Answer 19

True.

Question 20

What is the mechanism behind polyuria and polydipsia in a hypokalemic patient?

Answer 20

Impaired responsiveness to ADH (decreased expression of ADH-regulated aquaporin 2 water channels in the collecting duct).

Question 21

What are the effects of hypokalemia on the kidneys?

Answer 21

1. Decreased responsiveness to ADH (PU/PD)
2. Increased renal ammoniagenesis and urinary net acid excretion
3. Increased proximal renal tubular reabsorption (increased activity of the proximal Na+-H+ antiporter)
4. Decreased distal sodium reabsorption (decreased aldosterone secretion and direct effect of decreased ECF potassium concentration on the zona glomerulosa)

Question 22

What is the benefit of increased ammoniagenesis on acid-base imbalance during potassium depletion?

Answer 22

Decreased distal sodium reabsorption decreases K and H ion secretion by decreasing luminal electronegativity. This decreases potassium loss in the urine but also tends to impair renal acid excretion. Thus, increased renal ammoniagenesis during potassium depletion may represent a mechanism for enhancing urinary excretion of fixed acid (as NH4+) at a time when distal H ion secretion is impaired. Consequently, derangements in acid-base are minimized.

Question 23

Why can a patient experience an initial decrease in potassium concentration after infusion of potassium-containing fluids?

Answer 23

As a result of dilution, increased distal renal tubular flow, and cellular uptake of potassium (especially if the infused fluid also contains glucose).

Question 24

How would you give a bolus of KCl?

Answer 24

Total amount of KCl for bolus = (Ideal K – Observed K) x Estimated vascular volume

Give over 5-10 min diluted in equal or two times the volume with normal saline, through a central catheter.

Question 25

What changes on the ECG can we see in a patient with hyperkalemia?

Answer 25

- Increased amplitude and narrowing or “tenting” of the T waves (inconsistent in dogs and cats) - Shortening of QT-interval (abnormally rapid repolarization) - Prolongation of the PR-interval - Widening of the QRS complex - Decreases in the amplitude and widening of the P wave (impaired atrial conduction) - No P waves (severe hyperkalemia, atrial conduction ceases) - QRS complex merged with T wave (extreme hyperkalemia)  followed by ventricular fibrillation or asystole

Question 26

True or False: Increased potassium intake is a likely cause of sustained hyperkalemia in a healthy patient

Answer 26

False. It is unlikely to cause sustained hyperkalemia unless impaired renal excretion of potassium is present, or if iatrogenic causes.

Question 27

What type of metabolic acidosis (mineral vs organic) can cause hyperkalemia?

Answer 27

Mineral acidosis (NH4Cl and HCl) because it causes potassium to shift out of the cells in exchange for H+ ions that enter cells to be buffered. (In organic acidosis, lactate and ketoacid anions are more permeable and can follow H+ ions into the cell, so K+ do not need to be exchanged).

Question 28

Why hyperosmolality may cause hyperkalemia?

Answer 28

Because water moves from ICF to ECF and potassium follows because of solvent drag, and as a result of the increased ICF potassium concentration resulting from cellular water loss.

Question 29

What drugs can cause decreased potassium urinary excretion?

Answer 29

- ACEI - ARB - Cyclosporin and tacrolimus - Potassium-sparing diuretics (spironolactone, amiloride, triamterene) - NSAIDs - Heparin - Trimethoprim

Question 30

How can non-selective beta-blockers cause hyperkalemia?

Answer 30

They interfere with catecholamine-mediated uptake of potassium by liver and muscle by blocking beta2-adrenergic stimulation of cell membrane Na+,K+-ATPase.

Question 31

Give 3 examples of non-selective beta-blockers.

Answer 31

Propanolol, sotalol, timolol.

Question 32

What is the MOA of telmisartan and how can it cause hyperkalemia?

Answer 32

MOA: Antiogensin II receptor blocker (AT1 receptor) Hyperkalemia is caused by: - Decreased production of aldosterone  so there is impaired potassium excretion - Dilation of glomerular efferent arteriole  decreased delivery of sodium and water to the distal nephron and impaired renal potassium excretion

Question 33

How can NSAIDs cause hyperkalemia?

Answer 33

They inhibit prostaglandins, which stimulate renin release, so all the RAAS cascade is impaired. They may also impair the stimulatory effect of prostaglandins on potassium channels in the luminal membranes of renal tubular cells.

Question 34

List what treatment options do we have for a hyperkalemic patient, and what is their MOA?

Answer 34

- Calcium gluconate  To increase the threshold potential, thus normalizing the difference between the resting and the threshold potential and restoring normal membrane excitability. - Glucose/insulin  increasing endogenous insulin release, and moving potassium into cells. - Sodium bicarbonate  moving K+ ions into cells as H+ ions leave cells to titrate bicarbonate. +/- peritoneal dialysis, hemodialysis. Other options: - Loop or thiazide diuretics  increase the distal tubular flow rate and potassium secretion - Beta1-agonists (albuterol)  increase cellular uptake of potassium by stimulating Na+,K+-ATPase activity

Question 35

How can heparin cause hyperkalemia?

Answer 35

Impairs aldosterone production by decreasing the number and affinity of angiotensin II receptors in the zona glomerulosa of the adrenal gland.

Question 36

How can trimethoprim cause hyperkalemia?

Answer 36

Inhibits sodium channels in the luminal membranes of the principal cells.

Question 37

How can Cyclosporin A and tacrolimus cause hyperkalemia?

Answer 37

Decreased aldosterone production, inhibition of Na+,K+-ATPase, and interference with luminal potassium channels in renal tubular cells.