Electrolyte Disorders Flashcards
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
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
3
Q
Electrolyte Abnormality Treatment Goals
A
- Treat or prevent severe life-threatening signs and symptoms
- Improve or correct serum [electrolyte]
- Do not overcorrect
- Avoid undesirable side effects of treatment
- Correct underlying cause for abnormality
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
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
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
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
8
Q
Treating Hypokalemia
A
- Remove underlying cause if possible
- Replacement therapy in specific scenarios
- Evaluate and replace magnesium losses if present
9
Q
Hypokalemia Replacement Therapy Scenarios
A
- Symptomatic patients
- Underlying cardiac risk factors
- On digitalis glycoside
- Severe (K < 3)
- Ongoing loss of potassium
10
Q
Non-Pharm + Hypokalemia
A
- Potassium containing salt substitutes
- Dietary sources: fresh fruits, vegetables, meat
- Treat precipitating factor: diuretic therapy, vomiting, diarrhea
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
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
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
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
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
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
17
Q
Hyperkalemia Treatment Goals
A
- Antagonize adverse cardiac effects, if present
- Reverse other symptoms
- Return [serum] to normal
18
Q
Hyperkalemia Treatment Options
A
- Antagonism of K if cardiac abnormalities exist
- Promote intracellular redistribution
- Remove K from body
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
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
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
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
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
24
Q
Magnesium
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
Q
Magnesium ADME
A
- 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
Q
Hypomagnesaemia Etiologies
A
- 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
Q
Hypomagnesaemia Inducing Drugs
A
- Diuretics: thiazide and loop
- Amphotericin B
- Aminoglycosides
- Cisplatin
- Laxative anise
- Dextrose and insulin
28
Q
Hypomagnesemia Presentation
A
- Neuromuscular: hyperreflexia/tetany, tremors, seizures
- Cardiac: tachycardia, V. fib (torsade de pointes)
29
Q
Hypomagnesemia Treatment
A
- 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
Q
IV MgSO4 Replacement
A
- 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
Q
Oral Mg Replacement
A
- 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
Q
Serum Mg Levels + Mg Replacements
A
<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
Q
Hypermagnesemia Etiology
A
- Renal failure
- Adrenalcorticoid insufficiency
- Excessive intake: magnesium containing laxative abuse, over treatment with magnesium
34
Q
Hypermagnesemia Presentation
A
- 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
Q
Hypermagnesemia Treatment
A
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
Q
Calcium
A
- 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
Q
Corrected Calcium
A
-Use when albumin <4 g/dL
Corrected Ca = measured Ca + 0.8 * (4-measured albumin)
38
Q
Calcium Regulation
A
- 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
Q
Hypocalcemia Etiologies
A
- 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
Q
Hypocalcemia Inducing Drugs
A
- Loop diuretics
- Glucocorticoids
- Oral phosphates
- Calcitonin
- Bisphosphonates
- Citrated solutions
- Denosumab
- Phenobarbital, phenytoin (increase Vit D catabolism)
41
Q
Hypocalcemia Presentation
A
- Neuromuscular: tetany, muscle cramps
- CV: hypotension, decreased contractility, heart failure
- Neurologic: seizures, areflexia
- Delayed coagulation
- Bones: failure to mineralize bones/teeth, rickets and osteomalacia
42
Q
Hypocalcemia Signs
A
- 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
Q
Treating Severe/Symptomatic Hypocalcemia
A
- 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
Q
Treating Mild/Asymptomatic Hypocalcemia
A
- 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
Q
Hypercalcemia Etiologies
A
- Hyperparathyroidism
- Immobilization
- Malignancy in lung, breast, multiple myeloma (release PTH like peptide, metastases, other cytokines)
- Drug Induced
46
Q
Hypercalcemia Inducing Drugs
A
- Thiazide diuretics
- Lithium
- Calcium supplements
- Teriparatide (PTH analog)
- Vit D toxicity
- Vit A toxicity
47
Q
Hypercalcemia Presentation
A
- Acute: dehydration from not [urine], acute renal failure, coma, ventricular arrhythmias
- Chronic: metastatic calcification, nephrolithiasis, chronic renal insufficiency
48
Q
Severe Acute Hypercalcemia Treatment
A
-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
Q
Treating Chronic Hypercalcemia
A
- Calcitonin
- Bisphosphonates
- Oral phosphates
- Glucocorticoids
- Cinacalcet - decrease release of PTH
50
Q
Phosphorous
A
- 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
Q
Hypophosphatemia Etiologies
A
- Intracellular shifts: alkalosis, glucose/insulin, refeeding
- Inhibition/inadequate absorption: large amounts of calcium in diet
- Increased renal losses: hyper-PTH
52
Q
Hypophosphatemia Inducing Drugs
A
- Insulin, dextrose
- Catecholamines
- Parenteral nutrition - refeeding syndrome
- Sucralfate
- Aluminum antacids
- Calcium supplements
- Sevelamer
- Diuretics
53
Q
Hypophosphatemia Presentation
A
- 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
Q
Treating Severe/Symptomatic Hypophosphatemia
A
- <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
Q
Treating Asymptomatic/Less Severe Hypophosphatemia
A
- 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
Q
Hyperphosphatemia Etiologies
A
- Decreased elimination: renal failure, hypo-PTH
- Redistribution: tumor lysis syndrome, rhabdomyolysis, acidosis (lactic, ketoacidosis)
- Increased intake: Phosphate containing laxatives
57
Q
Hyperphosphatemia Presentation
A
- 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
Q
Hyperphosphatemia Treatment
A
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
