Lecture 3 Conditions of Potassium and Magnesium Imbalance

Question 1

Potassium daily intake and abundance within body, role

Answer 1

aily intake: 4700 mg (adequate) - most Canadians don’t reach this, foods with high this include fruits, vegetables, potatoes, milk, yogurt, bran cereals

most abundant IC cation

around 98% of total body this is within cells

actively transported into cells via ATPase

major determinant of resting action potential - neurons, skeletal muscle, cardiac myocytes

Question 2

Serum K+ levels, what is normal, what is it affected by?

Answer 2

normal is around 3.5-5 mmol/L

affected by dietary intake, excretion from kidneys (90%) and GI (10%), sequestration in muscle and hepatic cells, hormone levels (insulin, aldosterone), acid/base balance

Question 3

S&S of Hypokalemia

Answer 3

Mild: (3.0-3.5 mmol/L) - usually asymptomatic

Moderate (2.5-3.0 mmol/L) - muscle cramping, weakness, malaise, myalgias

Severe (<2.5 mmol/L) - ECG changes, arrhythmias (heart block, atrial flutter, paroxysmal atrial tachycardia), cramping, impaired muscle contraction

Question 4

Possible causes of hypokalemia

Answer 4

total body deficit - poor diet, excessive loss (ex. diarrhea, renal)

shift into IC compartment - metabolic alkalosis, insulin, B2 receptor agonists (epinephrine, salmeterol)

Question 5

What are some drugs that can induce hypokalemia?

Answer 5

diuretics (loop and thiazide) inhibit Na+ reabsorption ⇒ increase in [Na+] in distal tubule and collecting ducts ⇒ Na+ reabsorption in exchange for K+ - reduction in vascular volume will also stimulate release of aldosterone which works in distal tubule and collecting duct t promote Na+ reabsorption in exchange for K+

Insulin - promotes glucose uptake into cells ⇒ increase in K+ transport into liver, muscle, and adipose,, balanced with glucagon to regulate K+ levels

Decongestant (pseudoephedrine), caffeine, B2 receptor agonists ⇒ promote IC shift of K+

Question 6

What are some general rules when thinking about K+ supplementation for hypokalemia?

Answer 6

for every 1 mmol/L below 3.5 mmol/L the total body deficit is 100-400 mmol ⇒ in an acute care setting every 10 mmol of K+ supplementation should increase [K+] by 0.1 mmol/L

make sure to monitor [K+] frequently to avoid hyperkalemia, identify underlying med conditions (ex. HF), identify possible interactions: meds (ex. K+ sparing diuretics: spironolactone, triamterene, amiloride), med AEs potentiated by hypokalemia (ex. digoxin)

Question 7

Different oral K+ supplementation methods (meds)

Answer 7

potassium phosphate: use when pt is both hypokalemic and hypophosphatemic

potassium bicarbonate: use when pt is both hypokalemic and has metabolic acidosis

potassium chloride: most common salt for replacement therapy ⇒ available strengths are 8, 10, and 20 mEq, liquid formulations are cheapest option but have strong unpleasant taste, there are also wax-matrix tablets - Slow-K and generics, also controlled release microencapsulated - Micro-K Extendcaps and generics which have less GI irritation compared to wax-matrix

also has IV form - used when severely hypokalemic (<2.5 mmol/L), severe S&S of hypokalemia (ECG, muscle spasms), pt unable to tolerate oral ⇒ monitor ECG, high risk of overcorrecting, injection site pain and phlebitis ⇒ use saline-containing solutions for admin (dextrose solutions will cause insulin release and cause IC shift of K+)

Question 8

S&S of Hyperkalemia

Answer 8

generally related to cardiac, neuromuscular, and SMC fx,, Mild (5.1-5.9 mmol/L) - may be asymptomatic

Moderate (6-7 mmol/L) - cardiac arrhythmias (pt may sense heart palpitations)

Severe (>7 mmol/L) - cardiac arrhythmias, weakness, ascending paralysis, respiratory failure

Question 9

Possible causes of hyperkalemia

Answer 9

increased this intake - over correction of hypo

decreased excretion of this - acute or chronic renal failure, adrenal insufficiency

redistribution of this into EC space - metabolic acidosis

Question 10

What are some drugs that can induce hyperkalemia?

Answer 10

ACEIs, ARBs, direct renin inhibitors, mineralocorticoid receptor antagonists, K+ sparing diuretics, NSAIDs, B-blockers, digoxin, cyclosporine, tacrolimus, trimethoprim/sulfamethoxazole

Question 11

What is the management for mild-moderate hyperkalemia?

Answer 11

asymptomatic pt with <6 mmol/L and normal or mildly impaired renal fx usually respond well to diet changes, drug therapy changes (discontinue or lower dose of K+ sparing diuretic, K+ supplement, NSAID, ACEI, ARB)

can use furosemide to promote urinary K+ excretion

close follow-up of [K+], fluid volume status, and other electrolyte conc

Question 12

What is the management for severe hyperkalemia?

Answer 12

Calcium (admin IV) raises the cardiac threshold potential which antagonizes cardiac membrane effect of this

furosemide inhibits Na+ reabsorption from ascending loop of Henle which increases urinary K+ loss

insulin stimulates IC uptake of K+ - may require concurrent admin of dextrose

sodium bicarbonate raises serum pH (promotes IC shift of K+)

sodium polystyrene sulfonate (Kayexalate) cation exchange resin

hemodialysis will remove K+ from serum

Question 13

What is daily intake of Mg and what roles does it have in body, also serum conc levels, and renal excretion?

Answer 13

daily intake is 420 mg/day (men) and 320 mg/day women

predominantly an IC cation second most after K+

plays role in cellular fx - cofactor in BIOCH rxn especially those dependent on ATP

mitochondrial fxn, protein synthesis, glucose metabolism

serum conc - 0.7-1.0 mmol/L

excretion: mainly by kidneys, 95% of filtered this is reabsorbed, 20% in proximal tubule, 70% in thick ascending limb of loop of Henle ⇒ loop diuretics can cause profound loss of this through kidneys, also 10% in DCT

Question 14

S&S of Hypomagnesia

Answer 14

always check K+ conc with this as it may also be low

dominant organs: heart palpitations, cardiac arrhythmias, widening of QRS complex, sudden cardiac death

neuromuscular: tetany, twitching, generalized convulsions, Chvostek sign and Trousseau sign

Question 15

Possible causes of hypomagnesia

Answer 15

GI: reduce intake - malnutrition, alcoholism

reduced absorption - celiac, chronic PPI use

increased loss - excessive vomiting, excessive laxative use, prolonged diarrhea

Renal: glomerulonephritis, pyelonephritis

Drug induced: aminoglycosides, diuretics

Question 17

What is the management for hypomagnesia?

Answer 17

remembering to check Ca2+ and K+ levels as well cause they may also be low

> 0.5 mmol/L and asymptomatic: oral supplementation, common sources like oxide, hydroxide, chloride, citrate and gluconate salts - multiple doses required for all of them, most common dose-limiting side effect is diarrhea

<0.5 mmol/L or sx present: IV this sulfate should be admin

Question 18

Possible causes of hypermagnesia

Answer 18

rare condition, usually occurs in pt with advanced chronic kidney disease when this intake exceeds renal clearance

Drug induced: antacids and laxatives that contain this, lithium

Question 19

S&S of Hypermagnesia

Answer 19

usually asymptomatic if <2.0 mmol/L

lethargy, confusion, muscle weakness, dysrhythmias

Question 20

What is the management for hypermagnesia?

Answer 20

reduce this intake - stop or reduce use of antacids and laxatives

enhance elimination of this - furosemide 40 mg IV, forced diuresis (0.45% NaCl + loop diuretic)

antagonize the physiologic effect of it - Ca2+ IV