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Electrolyte Disorders Flashcards

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1
Q

Laboratory Electrolyte Tests

A
  • Chem 7: Na, Cl, BUN, K, HCO3, K, Creatinine, Glucose
  • Chem 10: Above + Calcium, magnesium, and phosphorous
  • Need to order ionized calcium separately
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2
Q

Electrolyte Abnormality Treatment Considerations

A
  • Symptom severity is related to the acuteness of the electrolyte abnormality
  • Slow/chronic onsets tend to be less aggressive and can be gradually corrected
  • Acute onsets tend to be more aggressive and need to be more aggressively treated
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3
Q

Electrolyte Abnormality Treatment Goals

A
  1. Treat or prevent severe life-threatening signs and symptoms
  2. Improve or correct serum [electrolyte]
  3. Do not overcorrect
  4. Avoid undesirable side effects of treatment
  5. Correct underlying cause for abnormality
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4
Q

Potassium

A
  • Main intracellular cation, only small amount in ECF (maintained by Na/K ATPase)
  • Normal: 3.5-5
  • Intracellular ~150 mEq/L
  • Functions in regulation of osmotic equilibrium, acid/base balance, transmission of nerve impulses, muscle contraction, glycogen, and protein synthesis
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5
Q

Potassium ADME

A
  • Abundant in diet and well absorbed via small intestine
  • Distribution primarily intracellular
  • Excretion: mainly renal (influenced by aldosterone), small amounts lost in feces and sweat
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6
Q

Etiologies of Hypokalemia

A
  • Redistribution: insulin, Beta-agonists, metabolic alkalosis (K decreases 0.6 for each 0.1 increase in blood pH)
  • Loss of potassium: GI losses (N/V, diarrhea, etc) or renal losses (mineralcorticoid excess
  • Poor intake/re-feeding syndrome
  • Drug induced: diuretics, insulin, glucocorticoids, amphotericin B
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7
Q

Hypokalemia

A
  • Decreases resting potential with no change in threshold, delayed repolarization
  • Muscle abnormalities: weakness, cramps, paralysis
  • Metabolic: hyperglycemia (decreased B-cell response to glucose) or metabolic alkalosis (increased HCO3 synthesis)
  • Cardiac Abnormalities: Bradycardia, heart block, PVCs, V tachycardia, V. fib, atrial flutters

ECG readings: ST depression, Flat t-waves, U-waves, widen PR and QRS interval

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8
Q

Treating Hypokalemia

A
  • Remove underlying cause if possible
  • Replacement therapy in specific scenarios
  • Evaluate and replace magnesium losses if present
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9
Q

Hypokalemia Replacement Therapy Scenarios

A
  • Symptomatic patients
  • Underlying cardiac risk factors
  • On digitalis glycoside
  • Severe (K < 3)
  • Ongoing loss of potassium
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10
Q

Non-Pharm + Hypokalemia

A
  • Potassium containing salt substitutes
  • Dietary sources: fresh fruits, vegetables, meat
  • Treat precipitating factor: diuretic therapy, vomiting, diarrhea
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11
Q

Pharm Therapy + Hypokalemia

A
  • Administer orally if possible
  • Divided doses better tolerated and safer
  • Continue replacement for several days to replete total body stores
  • Each 1 mEq under 3.5 represents a deficit of 100-400 mEq
  • KCl is most common replacement (Cl often loss in these patients too)
  • Caution in renally insufficient patients and those with redistribution to avoid hyperkalemia precipitation
  • Use Kacetate or Kcitrate in metabolic acidosis
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12
Q

Hypokalemia Pharm Dosing

A
  • Preventing Hypokalemia: start with 20 mEq/day
  • Treating Mild Hypokalemia: 40-100 mEq/day in divided doses
  • Treat severe deficiency: 120 mEq total dose
  • Doses >20mEq should be divided to minimize GI toxicity
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13
Q

Hypokalemia IV Treatments

A
  • Usually 10-20 mEq diluted in 100 mL sterile water or NS
  • Central line preferred, but can use the above [] in peripheral lines as well
  • 10mEq/hr max without ECG, 20mEq/hr max rate with ECG
  • *Can give 20 mEq/hr with closely monitored patients experiencing ECG changes from hypokalemia**
  • NO DEXTROSE SOLUTIONS: promotes insulin release which shifts K intracellularly
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14
Q

Measuring Serum K

A
  • Measure [serum] after each 30-40mEq increment for adults
  • Wait at least 30 minutes after K IV to re-measure K
  • Max [] for continuous peripheral IV replacement fluids is 80 mEq/L
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15
Q

Hyperkalemia Presentation

A
  • Cardiac abnormalities (life threatening): V fib., asystole
  • ECG: peaked T waves, widened QRS, increased PR interval
  • Muscle abnormalities similar to hypokalemia: weakness, paralysis
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16
Q

Hyperkalemia Etiologies

A
  • Renal Failure
  • Acidosis: metabolic acidosis, K increases 0.6 mEq for each 0.1 unit decrease in blood pH
  • Rhabdomyolysis
  • Mineralcorticoid deficiency
  • Drug Induced: K-sparing diuretics, ACE-I/ARBs, Heparin, NSAIDs, salt substitutes
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17
Q

Hyperkalemia Treatment Goals

A
  1. Antagonize adverse cardiac effects, if present
  2. Reverse other symptoms
  3. Return [serum] to normal
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18
Q

Hyperkalemia Treatment Options

A
  • Antagonism of K if cardiac abnormalities exist
  • Promote intracellular redistribution
  • Remove K from body
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19
Q

Hyperkalemia Treatment + Cardiac Effects

A
  • IV calcium gluconate or chloride
  • Restores normal conduction of heart but doesn’t reduce or redistribute K
  • Repeat doses if symptoms return
  • Only use calcium chloride for life threatening symptoms (1g IV push)
  • Gluconate: 1g IV over 2-3 minutes, repeating every 5 minutes until ECG normalizes
  • DON’T administer calcium if digoxin toxicity occuring
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20
Q

Hyperkalemia Treatment + Intracellular Redistribution

A
  • Regular insulin is first line to reduce K, NOT if patient has acidosis
  • 5-10 U IV or SQ
  • If glucose <250, give dextrose
  • Insulin promotes cellular uptake of K
  • Glucose enhances endogenous insulin release and prevents hypoglycemia
  • Albuterol is second line, use if unresponsive to insulin/glucose after 30-60 minutes
  • Nebulize 10 mg over 10 minutes
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21
Q

Hyperkalemia Treatment + Acidosis

A
  • Sodium bicarbonate, only used in hyperkalemic patients from metabolic acidosis
  • 50-100 mEq IV over 2-5 minutes
  • Don’t infuse on same line as parenteral nutrition or other Ca/Phos solutions
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22
Q

Hyperkalemia Treatment + Remove K

A
  • Loop diuretic if no severe renal impairment
  • Furosemide 20-40 mg IV (can repeat) or Bumetanide 0.5-1 mg IV
  • Sodium polystyrene sulfonate (Kayexalate)
  • Exchanges Na for K
  • 15-60 g orally, can administer rectally but less effective (sorbitol enhances elimination, associated with necrosis of large intestine)

-Hemodialysis

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23
Q

Hyperkalemia New Drugs

A
  • Patiromer (Veltassa): binds to K in exchanges for calcium, 8.4-25.2 gm PO QD
  • Sodium Zirconium cyclosilicate (Zs-9 Lokelma): polymer that exchanges K for Na, only for CHRONIC hyperkalemia
  • 10 gm PO TID x 2 days initially, 5-15 gm PO QD maintenance
  • All binding agents have potential significantly decrease the absorption of other oral medications, separate by other oral meds at least 6 hours if possible
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24
Q

Magnesium

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A
  • 2nd most abundant cation
  • <1% in ECF
  • Normal: 1.4-1.8 mEq/L
  • Functions: key roles in ATP synthesis and other phosphatases, ionic transport across membranes, cofactor in protein synthesis, mitochondrial oxidative metabolism, co-factor in multiple metabolic pathways
25
Magnesium ADME
- 1/3 ingested is absorbed - Dependent on serum Mg and decreased in presence of fat, calcium, and phytates - Eliminated primarily by kidneys (key role in regulating serum [Mg])
26
Hypomagnesaemia Etiologies
- Decreased intake/absorption: protein-calories malnutrition, TPN w/o Mg, alcoholism, malabsorption syndromes - Increased losses: GI losses, intestinal fistula, increased mineralcorticoids, increased PTH, drug-induced - Redistribution from re-feeding syndrome
27
Hypomagnesaemia Inducing Drugs
- Diuretics: thiazide and loop - Amphotericin B - Aminoglycosides - Cisplatin - Laxative anise - Dextrose and insulin
28
Hypomagnesemia Presentation
- Neuromuscular: hyperreflexia/tetany, tremors, seizures | - Cardiac: tachycardia, V. fib (torsade de pointes)
29
Hypomagnesemia Treatment
- Remove underlying cause - Magnesium replacement: oral if able to take and symptoms less severe, IV if severe or symptomatic - Potassium sparing diuretics: triamterene, amiloride, spironolactone
30
IV MgSO4 Replacement
- MgSO4 50%, 1gm/2mL = 8.1 mEq of Mg - Can also use MgCl 20% - 1gm/5Ml = 9.9mEq of Mg - Don't give rapidly unless having severe arrhythmia or seizure (causes hypotension, flush, sweating) - Dilute before administering to avoid pain and vein sclerosis - Only give IM if IV isn't available (painful) - Slow replacement allows for intracellular redistribution - Check serum Mg at least 4 hours after completing dose - Decrease doses for patient with renal failure
31
Oral Mg Replacement
- Milk of magnesia, magnesium containing antacids, magnesium oxide, gluconate - SE: diarrhea (main limiter) - Products differ significantly in amount of Mg per gram - Frequent dosing is necessary due to small quantities and GI intolerance
32
Serum Mg Levels + Mg Replacements
<1 mEq + Life-threatening symptoms - 1-2 g MgSO4, diluted, IV push over 1 minutes - Follow with 1mEq/kg LBW over 24 hours and 0.5 mEq/kg over next few days <1mEq w/o life-threatening symptoms - 1mEq/kg LBW over first 24 hours - 0.5 mEq/kg LBW over next few days >1 mEq/L w/o symptoms -Magnesium oxide 400 mg PO QID
33
Hypermagnesemia Etiology
- Renal failure - Adrenalcorticoid insufficiency - Excessive intake: magnesium containing laxative abuse, over treatment with magnesium
34
Hypermagnesemia Presentation
- Neuromuscular: neuromuscular blockage, muscle weakness, respiratory muscle paralysis - CV: hypotension, sinus bradycardia, heart block, asystole - Nervous System: loss of deep tendon reflexes, somnolence, coma
35
Hypermagnesemia Treatment
Calcium - Antagonizes neuromuscular and CV effect of magnesium - Calcium gluc 1 gm administered slow IV push - Calcium chloride 1gm for life-threatening symptoms - Rapid onset, transient duration, may need to repeat - Add loop diuretics and saline if normal renal fxn - Hemodialysis in renal failure - May need mechanical ventilation, vasopressors, and cardiac pacemakers until [serum] decrease
36
Calcium
- Most abundant mineral in body - <1% in ECF, normal serum levels 8.5-10 mg/dL - Low serum albumin leads to decreased serum calcium (~50% protein bound) - Increased pH causes increased protein binding - Measured ionized (Free) Ca: normally 4.4-5.4 Functions - Structural support for bones and teeth - Clotting: clotting cascade, platelet activation - Muscle contraction - Secretion of hormones - Pacemaker activity in heart - Release of neurotransmitters
37
Corrected Calcium
-Use when albumin <4 g/dL Corrected Ca = measured Ca + 0.8 * (4-measured albumin)
38
Calcium Regulation
- PTH decreases Ca when stimulated by increasing intestinal, renal, and bone absorption - Vit D increases GI absorption and increases bone response to PTH - Calcitonin stimulates increases in Ca by inhibiting bone resoprtion and increasing excretions
39
Hypocalcemia Etiologies
- Hypoparathyroidism - Parathyroidectomy, thyroidectomy ('Hungry Bone Syndrome') - Vitamin D deficiency - Inadequate conversion of Vit D to active form (renal failure) - Pancreatitis - Decreases intake/malabsorption (increased dietary protein/phosphorous) - Hypomagnesemia - inhibits PTH - Alkalosis: increased protein binding
40
Hypocalcemia Inducing Drugs
- Loop diuretics - Glucocorticoids - Oral phosphates - Calcitonin - Bisphosphonates - Citrated solutions - Denosumab - Phenobarbital, phenytoin (increase Vit D catabolism)
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Hypocalcemia Presentation
- Neuromuscular: tetany, muscle cramps - CV: hypotension, decreased contractility, heart failure - Neurologic: seizures, areflexia - Delayed coagulation - Bones: failure to mineralize bones/teeth, rickets and osteomalacia
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Hypocalcemia Signs
- Chvostek's sign: twitching of facial muscles when tap on facial nerve anterior to ear - Trousseau's sign: carpal spasm elicited when a BP cuff is inflated above systolic BP for 3 minutes - ECG: prolonged QT interval
43
Treating Severe/Symptomatic Hypocalcemia
- IV Calcium: 2-3 gm of gluconate or 1 g of chloride - Calcium Gluc 10% (90 mg of Ca) - less likely to cause IV/soft tissue irritation, can push IV, dilute if possible - Calcium Chloride 10% (270 mg Ca) - only for severe, life threatening symptoms, IV push and dilute when possible - Replete Ca with continuous infusion 0.5-2 mg/kg/hr - Monitor serum Ca every 4-6 hours
44
Treating Mild/Asymptomatic Hypocalcemia
- Oral calcium: 1-3 g/day of elemental calcium in divided doses to increase absorption - Vit D may also be needed to enhance absorption: Cholecalciferol or Ergocalciferol (1,25 dihydroxyD3 if chronic renal disease) - Thiazide diuretics - Measure magnesium and replace if low
45
Hypercalcemia Etiologies
- Hyperparathyroidism - Immobilization - Malignancy in lung, breast, multiple myeloma (release PTH like peptide, metastases, other cytokines) - Drug Induced
46
Hypercalcemia Inducing Drugs
- Thiazide diuretics - Lithium - Calcium supplements - Teriparatide (PTH analog) - Vit D toxicity - Vit A toxicity
47
Hypercalcemia Presentation
- Acute: dehydration from not [urine], acute renal failure, coma, ventricular arrhythmias - Chronic: metastatic calcification, nephrolithiasis, chronic renal insufficiency
48
Severe Acute Hypercalcemia Treatment
-Increase urinary calcium excretion by infusing with NS and beginning loop diuretics after rehydrating Monitor for co-existing electrolyte abnormalities -Deccrease bone resorption with calcitonin (SE: tachyphylaxis), IV bisphosphonates (delayed onset), or glucocorticoids
49
Treating Chronic Hypercalcemia
- Calcitonin - Bisphosphonates - Oral phosphates - Glucocorticoids - Cinacalcet - decrease release of PTH
50
Phosphorous
- 2nd most abundant mineral in body - >80% is complexed with Ca in bones/teeth - other 20% is metabolically active, mostly intracellularly - Normal: 2.5-4.5 (doesn't reflect total body stores) - Eliminated renally - Closely linked to calcium regulation - Functions: cellular membranes, energy transfer, 2,3 DPG in RBC, intracellular buffer
51
Hypophosphatemia Etiologies
- Intracellular shifts: alkalosis, glucose/insulin, refeeding - Inhibition/inadequate absorption: large amounts of calcium in diet - Increased renal losses: hyper-PTH
52
Hypophosphatemia Inducing Drugs
- Insulin, dextrose - Catecholamines - Parenteral nutrition - refeeding syndrome - Sucralfate - Aluminum antacids - Calcium supplements - Sevelamer - Diuretics
53
Hypophosphatemia Presentation
- Muscle weakness: diaphragm fatigue/failure, decreased cardiac contractility, skeletal muscle weakness - Hemolytic anemia - Rhabdomyolysis - GI: anorexia, N/v - CNS: malaise, irritability, paresthesias, obtundation, coma, seizures
54
Treating Severe/Symptomatic Hypophosphatemia
- <1 mg/dL: wide range of doses for repletion - Infuse 0.25 mM/kg LBW IV over 4-12 hours - Allow for redistribution and remeasure levels - Generally need to repeat over several days to prevent recurrence
55
Treating Asymptomatic/Less Severe Hypophosphatemia
- Oral phosphates - Give supplements in divided doses: 1-2 g in 3-4 divided doses per day - SE: GI, diarrhea - Usually need to continue after serum levels normalize to replete stores - Limited number of options: Phos-NaK that needs to be diluted before admission
56
Hyperphosphatemia Etiologies
- Decreased elimination: renal failure, hypo-PTH - Redistribution: tumor lysis syndrome, rhabdomyolysis, acidosis (lactic, ketoacidosis) - Increased intake: Phosphate containing laxatives
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Hyperphosphatemia Presentation
- Signs due to hypocalcemia/precipitation of salt crystals - Precipitation occurs when Serum Ca * Phos > 50-60 - Deposits crystals in joints, soft tissue, and kidney which can lead to renal failure secondary to obstructive uropathy - GI disturbances and CNS symptoms can also occur (N/V, diarrhea, lethargy, seizure) - Chronic elevations of phosphorous depress Ca and leads to metabolic bones disease
58
Hyperphosphatemia Treatment
Severe (hypocalcemia symptoms) -Treat with IV calcium salts even if exceeds Ca *Phos solubility Less Severe (decrease absorption/increase elimination) - Oral phosphate binders to decrease GI absorption (Ca/Mg/Al salts, lanthium carbonate, sevelamer) - Dialysis - Hydration and diuretics
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