Potassium

Question 1

What 8 factors affect internal K+ balance?

Answer 1

• Insulin - high K+ in blood stimulates pancreas to make insulin –> inc K+ uptake into liver and muscle cells –> dec K+ in blood
• Aldosterone - stimulates K+ uptake by cells (little effect)
• Catecholamines - stimulate uptake of K+ into cell by activation of Na-K pump thru B2 receptors
• Acid/Base Balance
  
  • In acidemia… H+ enters cell and K+ leaves
  • In alkalosis … H+ leaves cells and K+ enters
• Plasma Tonicity - if high plasma tonicity, water moves out of cell and takes K+ w/ it (solvent drag)
• Cell Lysis - K+ that was inside that cell is now released into extracellular space
• Cell Proliferation - if rapid, K+ taken up into these new cells –> dec K+ in extracellular space
• Cell Membrane Disorders - skeletal muscle membrane ion channel defects –> flaccid paralysis and transmembrane K+ shifts
  
  • Hyperkalemic periodic paralysis - Na channel defect
  • Hypokalemic periodic paralysis - Ca channel defect

Question 2

How is external K+ balance maintained?

Answer 2

• K+ intake (diet, tpa nutrition, IV w/ K+ in it, drugs like penicillin, blood transfusions, herbal meds like alfalfa, dandelion, noni juice)
• K+ excretion
  • 90% kidney (under strict regulation)
  • 10% stool and sweat

Question 3

How does the kidney handle K+?

Answer 3

• Prox tubule - 65%; passive reabsorption
• TAL - via Na-K-2Cl and Na-K pump
• CD - where most of the regulation occurs
  
  • P cells - ENaC, ROMK (voltage-dep), BK (flow-dep) and Na-K pump
  • I cells - just BK and Na-K pump

Question 4

How does aldosterone affect K+ excretion?

Answer 4

• binds internal receptor in distal nephron –> transcriptional inc in Na-K, ENaC and apical K+ channels
• No “aldosterone escape” for K+ like that of Na+; K+ excretion remains high w/ persistent aldosterone

Question 5

How do flow rate, Na+ delivery and anion composition in distal nephron affect K+ excretion?

Answer 5

• Flow Rate - high flow activate BK channel and maintains low K+ in lumen b/c constantly moving in new low-K fluid; creates gradient for K+ secretion (inc secretion)
• Distal Tubular Na Delivery - more Na+ delivered to distal tubule –> more Na reabsorption –> electrochemical gradient that powers ROMK (inc K+ secretion)
• Distal Tubular Anion Composition - Cl- flow has opp. effect; dec Cl- delivery (b/c sub another anion) –> this new anion is not as well reabsorbed –> stay in lumen making it more neg –> enhance electrochemical gradient –> ROMK

Question 6

How does extracellular pH affect K+ excretion?

Answer 6

DEC (makes it harder to excrete K+)

Question 7

How does serum K+ conc affect K+ excretion?

Answer 7

• Body adapts to inc K+ in plasma alone by inc Na-K activity, inc ENaC and apical K channels and inc overall SA of basolateral membrane all in principal cells
• Also dec K+ reabsorption in intercalated cells

Question 8

What are the ECG and muscle changes in hyperkalemia?

Answer 8

• ECG Changes
  
  • Peaked T waves
  • Wide QRS/prolonged PR (makes sense b/c hyperkalemia slows conduction)
    
    • Hyperkalemia = less K+ in cell = less neg RMP = not as many channels are able to open = slower conduction
  • Eventually sine-wave morphology
• Muscular weakness, quadriplegia, respiratory arrest

Question 9

4 Steps to Hyperkalemia Tx

Answer 9

1- Membrane stabilization - IV Ca+ inc threshold potential for quick reversal of ECG changes; no actual effect on K+ in blood

2- Redistribute K+ into cell
- IV insulin, IV sodium bicarb, beta agonists

3- Enhance elimination of K+

    - Inc urine flow & inc Na delivery - diuretics, IV saline
    - GI ion exchange resins (syrup you drink);Kayexalate
    - Acute hemodialysis

4- If chronic… dec K+ intake, treat underlying cause, stop offending drugs, diuretics, mineralocorticoid replacement (rare)

Question 10

What are the ECG and kidney changes in hypokalemia?

Answer 10

• ECG Changes
  
  • Flat t waves
  • Prominent U wave (downward deflection in middle of t wave)
  • Depressed ST segment
• In kidney… exchange K+ for H+ so high H+ in tubular cells –> ammoniagenesis

Question 11

Hypokalemia Tx

Answer 11

• Treat underlying cause
• K+ replenishment
  
  • Do not want it to be too rapid –> transient hyperkalemia is cardiotoxic and musc toxic
  • 10 mEq/hr
• K-sparing diuretics if hypokalemia w/ HTN

Question 12

Hypertensive v. Hypotensive Hypokalemia

Answer 12

HYPER

• Hyper-renin-emia (renal artery stenosis, renin-secreting tumor)
• Primary hyperaldosteronism (Conn’s)
• Cushing’s - exogenous steroids cross react w/ MR receptors
• Congenital adrenal hyperplasia

HYPO

• Diuretic use
• Osmotic diuretucs - inc glucose in urine - water enters urine and J+ follows
• Renal tubular acidosis (types I and II)
• Prolonged drainage or vomiting
• Ureteral diversion (divert urine into ileum or colon due to disease –> exchange K+ for Na and Cl- in intestine)

Question 13

Causes of Hyperkalemia

Answer 13

Impaired External Balance

- Excess K+ intake w/o proper kidney excretion
- Dec renal excretion
    - Renal insufficiency - dec GFR - dec K+ filtered load; or other defect in kidney handling
    - Dec distal tubular flow/ Na delivery - actual vol depletion, dec EABV, meds (NSAIDs, ACEi/aldosterone-receptor blockers)
    - Mineralocorticoid deficiency - can be Addison's (autoimmune adrenal attack), DM, drug-induce hypo-aldosteronism
    - Distal tubular dysfunction - nephritis, sickle cell, K-sparing diuretics (dec ENaC which dec ROMK)

Impaired Internal Balance

- Insulin def - DM
- B-blockade- beta blockers --> dec Na-K pump efficiency
- Hypertonicity - as in hyperglycemia --> solvent drag
- Acidemia
- Cell Lysis

Question 14

Causes of Hypokalemia

Answer 14

Impaired External Balance

- Inadequate K+ intake
- Inc extra-renal K+ loss (laxatives, drainage, vomiting)
- Inc renal K+ loss (potassium wasting)
    - W/ HTN
    - W/o HTN

Impaired Internal Balance

- Insulin excess - if insulin therapy
- Catecholamine excess - MI, delirium, excessive agonist use (asthma inhaler)
- Alkalemia
- Cell proliferation