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DiBart 2021 > Chapter 5: Potassium > Flashcards

Chapter 5: Potassium Flashcards

1
Q

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

A

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

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2
Q

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

A
  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
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3
Q

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

A

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

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4
Q

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

A

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

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5
Q

How do loop diuretics affect K+ reabsorption?

A

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

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6
Q

What hormone stimulates the electrogenic Na channel

A

Aldosterone

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7
Q

How does the electrogenic Na channel enhance K+ excretion?

A

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

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8
Q

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

A

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

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9
Q

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

A

bicarb secretion –> base secretion

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10
Q

What are the 3 determinants of K+ excretion?

A
  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
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11
Q

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

A

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

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12
Q

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

A

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
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13
Q

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

A

Serum, because platelets release potassium during the clotting process.

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14
Q

What conditions can cause pseudohyperkalemia?

A

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

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15
Q

What is the formula for potassium fractional excretion?

A

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

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16
Q

What are the main causes of hypokalemia?

A
  • Decreased intake
  • Translocation (ECF –> ICF)
  • Increased loss
17
Q

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

A

False, it leads to metabolic acidosis.

18
Q

Under which potassium concentration can you see frank rhabdomyolysis?

A

Less than 2 mEq/L.

19
Q

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

A

True.

20
Q

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

A

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

21
Q

What are the effects of hypokalemia on the kidneys?

A
  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)
22
Q

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

A

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.

23
Q

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

A

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

24
Q

How would you give a bolus of KCl?

A

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.

25
Q

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

A
  • 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
26
Q

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

A

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

27
Q

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

A

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).

28
Q

Why hyperosmolality may cause hyperkalemia?

A

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.

29
Q

What drugs can cause decreased potassium urinary excretion?

A
  • ACEI
  • ARB
  • Cyclosporin and tacrolimus
  • Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
  • NSAIDs
  • Heparin
  • Trimethoprim
30
Q

How can non-selective beta-blockers cause hyperkalemia?

A

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

31
Q

Give 3 examples of non-selective beta-blockers.

A

Propanolol, sotalol, timolol.

32
Q

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

A

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

33
Q

How can NSAIDs cause hyperkalemia?

A

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.

34
Q

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

A
  • 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
35
Q

How can heparin cause hyperkalemia?

A

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

36
Q

How can trimethoprim cause hyperkalemia?

A

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

37
Q

How can Cyclosporin A and tacrolimus cause hyperkalemia?

A

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

DiBart 2021 (9 decks)

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